Methods of treatment using an Anti-abeta protofibril antibody

Abstract

Disclosed herein are methods of selecting, monitoring, and treating subjects with Alzheimer's disease (AD) or suspected of having AD or another disorder associated with amyloid accumulation in the brain based on the risk of an ARIA event or brain hemorrhage. Also disclosed herein are methods of treating subjects having or suspected of having AD comprising subcutaneously administering an anti-Aβ protofibril antibody.

Description

Attorney Docket No.08061.0062-00304 METHODS OF TREATMENT USING AN ANTI-Aβ PROTOFIBRIL ANTIBODY RELATED APPLICATIONS This application claims the benefit of and priority to US Provisional Application Serial No.63 / 507,400, filed June 9, 2023, US Provisional Application Serial No.63 / 572,110, filed March 29, 2024, and US Provisional Application Serial No.63 / 648,077, filed May 15, 2024, the contents of each of which are incorporated herein by reference in their entirety. FIELD Disclosed herein are methods and dosing regimens for treating Alzheimer’s disease (AD) in a subject with an anti-Aβ protofibril antibody, as well as methods relating to amyloid related imaging abnormalities (ARIA). BACKGROUND Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder of unknown etiology and the most common form of dementia among older people. In 2006, there were 26.6 million cases of AD in the world (range: 11.4-59.4 million) (Brookmeyer, R., et al., Forecasting the global burden of Alzheimer’s Disease. Alzheimer Dement.2007; 3:186-91), while there were more than 5 million people in the United States reportedly living with AD (Alzheimer’s Association, Alzheimer’s Association report, 2010 Alzheimer’s disease facts and figures. Alzheimer Dement.2010; 6:158-94). By the year 2050, the worldwide prevalence of AD is predicted to grow to 106.8 million (range: 47.2-221.2 million), while in the United States alone the prevalence is estimated to be 11 to 16 million. (Brookmeyer, supra, and 2010 Alzheimer’s disease facts and figures, supra). The disease generally involves a global decline of cognitive function that progresses slowly and leaves end-stage subjects bedridden. AD subjects typically survive for only 3 to 10 years after symptom onset, although extremes of 2 and 20 years are known. (Hebert, L.E., et al., Alzheimer disease in the U.S. population: prevalence estimates using the 2000 census. Arch Neurol.2003; 60:1119-1122.) AD is the seventh leading cause of all deaths in the United States and the fifth leading cause of death in Americans older than the age of 65 years, despite the fact that mortality due to AD is greatly underestimated because death certificates rarely attribute the cause of death to AD. (Alzheimer’s Association. Alzheimer’s Association report.2010 Alzheimer’s disease facts and figures. Alzheimer Dement.2010; 6:158-94.) AD represents a significant economic burden across industrialized countries with a substantial impact on healthcare systems and the public purse as well as on subjects and their families. In the United States alone, total payments for 2010 were estimated at $172 billion, including $123 billion for Medicare and Medicaid.Attorney Docket No.08061.0062-00304 Histologically, the disease is characterized by neuritic plaques, found primarily in the association cortex, limbic system and basal ganglia. The major constituent of these plaques is amyloid beta peptide (Aβ). Aβ exists in various conformational states - monomers, oligomers, protofibrils, and insoluble fibrils. Details of the mechanistic relationship between onset of Alzheimer’s disease and Aβ production is unknown. However, some anti-Aβ antibodies are undergoing clinical study now as potential therapeutic agents for Alzheimer’s disease. Despite the recent development of treatments for AD, including those targeting Aβ, there remains a need for better treatments, including more refined methods of selecting patients suitable for treatment and calibrating responses to treatment events such as ARIA. Accordingly, disclosed herein are improved methods of selecting, monitoring, and treating patients with AD to treat patients less likely to exhibit ARIA and / or to address response to incidences of ARIA during treatment. SUMMARY One aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). A further aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ IDAttorney Docket No.08061.0062-00304 NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). Another aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and / or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg. In some embodiments, the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg. In some embodiments, the dose is administered in two parts, e.g., consecutively. In some embodiments, the anti-Aβ protofibril antibody is administered once weekly. In some embodiments, the anti-Aβ protofibril antibody is administered once biweekly. In some embodiments, the anti-Aβ protofibril antibody is administered once monthly. In some embodiments, the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen. In some embodiments, the initiation dosing regimen comprises intravenous administration of each initiation dose or subcutaneous administration of each initiation dose. In some embodiments, the maintenance dosing regimen comprises subcutaneous administration of each maintenance dose or intravenous administration of each maintenance dose.Attorney Docket No.08061.0062-00304 In some embodiments, the initiation dosing regimen comprises at least one initiation dose administered intravenously and at least one initiation dose administered subcutaneously. In some embodiments, the maintenance dosing regimen comprises at least one maintenance dose administered intravenously and at least one maintenance dose administered subcutaneously. In some embodiments, the initiation dose is greater than the maintenance dose. In some embodiments, the initiation dose of the anti-Aβ protofibril antibody is 150 mg to 600 mg, e.g., 200 mg to 550 mg, preferably 500 mg, administered subcutaneously. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody is 150 mg to 500 mg, e.g., 360 mg, administered subcutaneously. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody is 250 mg administered subcutaneously. In some embodiments, the initiation dose is administered weekly. In some embodiments, the maintenance dose is administered weekly. In some embodiments, the maintenance dose is administered biweekly. In some embodiments, the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months. In some embodiments, the first time period is at least 18 months. In some embodiments, the first time period is at least 24 months. In some embodiments, the first time period lasts until the subject is amyloid negative. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 24 months, and then subcutaneously administered at a maintenance dose of 250 mg biweekly for the second period of time. In some embodiments, the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression. In some embodiments, the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject.Attorney Docket No.08061.0062-00304 In some embodiments, the maintenance dose is subcutaneously administered with an autoinjector (AI). In some embodiments, the anti-Aβ protofibril antibody is intravenously administered at a dose of 10 mg / kg relative to the weight of the subject, biweekly. In some embodiments, the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe. In some embodiments, the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition via an autoinjector. In some embodiments, the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. In some embodiments, the anti-Aβ protofibril antibody is BAN2401 (lecanemab). In some embodiments, the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment. In some embodiments, the change and / or difference in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42 / 1- 40 and / or increased total tau, p-tau (e.g., p-tau181, p-tau217, and / or p-tau231), the ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). In some embodiments, the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology during and / or after treatment. In some embodiments, the change and / or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42 / 1- 40 and / or decreased total tau, p-tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or decreased totalAttorney Docket No.08061.0062-00304 tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). In some embodiments, the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), a CSF assessment of total tau, a CSF assessment of p-tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217), MRI, retinal amyloid accumulation, and / or a blood biomarker assessment (e.g. a plasma Aβ1-42 / 1-40 ratio, plasma p-tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217). In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is monitored for development of ARIA. In some embodiments, the subject is 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. In some embodiments, the subject has Alzheimer’s disease. In some embodiments, the subject has early Alzheimer’s disease. In some embodiments, the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject is suspected of having AD. In some embodiments, the subject is a subject at risk for developing AD. In some embodiments, the subject at risk for developing AD has pre-AD. In some embodiments, the subject does not have cognitive impairment.Attorney Docket No.08061.0062-00304 In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. In some embodiments, the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. An aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering toAttorney Docket No.08061.0062-00304 the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 18 months. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 24 months. In some embodiments, the maintenance dose of the antibody is administered weekly. In some embodiments, the maintenance dose of the antibody is administered biweekly. In some embodiments, the maintenance dose of the antibody is administered using a vial- syringe. In some embodiments, the maintenance dose of the antibody is administered using an AI. One aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarityAttorney Docket No.08061.0062-00304 determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: subcutaneously administeringAttorney Docket No.08061.0062-00304 the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 18 months. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 24 months. In some embodiments, the initiation dose of the antibody is administered using a vial- syringe. In some embodiments, the initiation dose of the antibody is administered using an AI. In some embodiments, the maintenance dose of the antibody is administered weekly. In some embodiments, the maintenance dose of the antibody is administered biweekly. In some embodiments, the maintenance dose of the antibody is administered using a vial- syringe. In some embodiments, the maintenance dose of the antibody is administered using an AI. In some embodiments, the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. In some embodiments, the anti-Aβ protofibril antibody is BAN2401 (lecanemab). In some embodiments, the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. In some embodiments, the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42 / 1-40, and / or increased total tau, p-tau (e.g, p-tau181, p-tau217, and / or p-tau231), ratio of p-tau181 / np-tau181, ratio of p-tau217 / np-tau217, neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P- tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231, ratio of p-tau181 / np-tau181, ratio of p- tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL).Attorney Docket No.08061.0062-00304 In some embodiments, the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology during and / or after treatment. In some embodiments, the change and / or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42 / 1- 40 and / or decreased total tau, p-tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p- tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p-tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). In some embodiments, the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation. In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is monitored for development of ARIA. In some embodiments, the subject is 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. In some embodiments, the subject has Alzheimer’s disease. In some embodiments, the subject has early Alzheimer’s disease. In some embodiments, the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinicalAttorney Docket No.08061.0062-00304 criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject is suspected of having AD. In some embodiments, the subject is a subject at risk for developing AD. In some embodiments, the subject at risk for developing AD has pre-AD. In some embodiments, the subject does not have cognitive impairment. In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. In some embodiments, the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. A further aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regionsAttorney Docket No.08061.0062-00304 (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject;Attorney Docket No.08061.0062-00304 or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg. In some embodiments, the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe. In some embodiments, the subcutaneously administered maintenance dose of the antibody is administered using an AI. In some embodiments, the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab. In some embodiments, the first anti-Aβ antibody is donanemab. Another aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg / kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 250 mg. In some embodiments, the subject is on a thrombolytic or anti-platelet agent but not an anticoagulant. In some embodiments, the subject is receiving an anti-platelet medication. In some embodiments, the subject is receiving a thrombolytic agent. In some embodiments, the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent. In some embodiments, the subject is receiving aspirin. In some embodiments, the subject is receiving a fibrinolytic. In some embodiments, the subject has had or is at an increased risk for a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment. In some embodiments, the subject has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment.Attorney Docket No.08061.0062-00304 Enumerated Embodiments 1. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject does not have a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, prior to treatment and / or wherein the subject has not exhibited a change, e.g., a decrease in brain white matter as measured by brain imaging prior to the treatment. 2. A method of selecting a subject having AD, suspected of having AD, or at risk for AD, for treatment with an anti-amyloid β (Aβ) protofibril antibody, comprising: a. determining that the subject has not had and / or does not currently have a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, and / or has not exhibited a change, e.g., a decrease, in brain white matter as measured by brain imaging prior to the treatment; b. selecting the subject for treatment with a therapeutically effective dose of the anti-amyloid β (Aβ) protofibril antibody. 3. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is on a thrombolytic or anti-platelet agent but not an anticoagulant. 4. The method of embodiment 3, wherein the subject is receiving an anti-platelet medication. 5. The method of embodiment 3, wherein the subject is receiving a thrombolytic agent. 6. The method of embodiment 5, wherein the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent. 7. The method of embodiment 6, wherein the subject is receiving aspirin. 8. The method of embodiment 6, wherein the subject is receiving a fibrinolytic. 9. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is not treated with an anticoagulant. 10. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is at an increased risk of an ARIA event or brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, the method further comprising administering a steroid and / or monitoring the subject’s brain (e.g., by MRI).Attorney Docket No.08061.0062-00304 11. The method of embodiment 10, wherein the subject has had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event prior to treatment. 12. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, detecting an ARIA event, e.g., a severe ARIA event, ARIA- H, ARIA-E, and administering a steroid. 13. The method of any one of embodiments 1-12, wherein the method reduces brain amyloid. 14. A method of treating severe ARIA in a subject receiving an anti-amyloid β (Aβ) protofibril antibody, the method comprising administering a steroid and / or monitoring the subject’s brain (e.g., by MRI). 15. The method of any one of embodiments 1-14, wherein the anti-Aβ protofibril antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6 (LCDR3). 16. The method of any one of embodiments 1-15, wherein the anti-Aβ protofibril antibody comprises a heavy chain variable region comprising an amino acid sequence of SEQ ID NO: 7 and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 8. 17. The method of any one of embodiments 1-16, wherein the anti-Aβ protofibril antibody comprises BAN2401 (lecanemab). 18. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises an intravenous infusion of 10 mg / kg relative to the weight of the subject. 19. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of about 250 to 720 mg. 20. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 250 mg. 21. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 360 mg. 22. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 500 mg.Attorney Docket No.08061.0062-00304 23. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 720 mg. 24. The method of any one of embodiments 1-19, wherein the therapeutically effective dose is administered subcutaneously by an autoinjector. 25. The method of any one of embodiments 1-18, wherein the therapeutically effective dose is administered weekly. 26. The method of any one of embodiments 1-17 and 19-24, wherein the therapeutically effective dose is administered every 2 weeks. 27. The method of any one of embodiments 1-26, wherein the frequency of administration is reduced after 18 months of treatment, e.g., to a frequency of every 2, 4, 6, 8, 10, or 12 weeks. 28. The method of any one of embodiments 1-27, wherein the therapeutically effective dose is reduced after 18 months of treatment, e.g., to a dose of 360 mg administered subcutaneously, or 250 mg administered subcutaneously, or maintained at a dose of 10 mg / kg administered intravenously. 29. The method of any one of embodiments 22 or 24-28, wherein the therapeutically effective dose is reduced from a weekly dose of 500 mg administered subcutaneously to a weekly dose of 360 mg administered subcutaneously, or 250 administered subcutaneously. 30. The method of any one of embodiments 24-28, wherein the therapeutically effective dose is reduced from a weekly dose of 720 mg administered subcutaneously to a weekly dose of 360 mg administered subcutaneously, or 250 administered subcutaneously 31. The method of any one of embodiments 1-30, wherein the subject is sequentially or simultaneously administered a second therapeutic agent. 32. The method of embodiment 31, wherein the second therapeutic agent is an anti-tau antibody. 33. The method of embodiment 32, wherein the anti-tau antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO:15 (HCDR1), SEQ ID NO:16 (HCDR2), SEQ ID NO:17 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO:18 (LCDR1), SEQ ID NO:19 (LCDR2), and SEQ ID NO:20 (LCDR3). 34. The method of embodiment 32 or 33, wherein the anti-tau antibody or antigen binding fragment thereof comprises a heavy chain variable region of SEQ ID NO: 21 and a light chain variable region of SEQ ID NO: 22. 35. The method of any one of embodiments 1-34, wherein the method further comprises monitoring for ARIA, e.g., ARIA-E and / or ARIA-H, e.g., as observed by MRI.Attorney Docket No.08061.0062-00304 36. The method of any one of the embodiments 1-35, wherein the method does not require a titration step prior to administering to the subject a first therapeutically effective dose of the anti-Aβ protofibril antibody. 37. The method of any one of embodiments 1-36, wherein the method results in: a. an improvement or slowing of worsening of one or more cerebrospinal fluid biomarkers, e.g., Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, p-tau (e.g., p-tau181, p-tau217, and / or p-tau231), the ratio of p-tau181 / np-tau181, the ratio of p-tau217 / np-tau217, neurogranin, neurofilament light (NfL) peptide, phosphorylated tau; and / or b. a reduction or a slowing of increase of plasma or serum biomarkers, e.g., Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, phosphorylated tau (P-tau) (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), 231 (P-tau231)), the ratio of P-tau181 / NP- tau181, and / or the ratio of P-tau217 / NP-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light (NfL); as compared to before treatment and / or as compared to an untreated control subject. 38. The method of any one of embodiments 1-37, wherein the treatment a. delays clinical decline as determined by ADCOMS; b. delays clinical decline as determined by ADAS MCI-ADL; c. delays clinical decline as determined by modified iADRS; d. delays clinical decline as measured by a CDR-SB; or e. delays clinical decline as measured by an ADAS-Cog. 39. The method of embodiment 37 or embodiment 38, wherein the result is measured at least 6 months after administration of a first therapeutically effective dose. 40. The method of any one of embodiments 37-39, wherein the result is measured at least 12 months after administration of a first therapeutically effective dose. 41. The method of any one of embodiments 37-39, wherein the result is measured at least 13 months after administration of a first therapeutically effective dose. 42. The method of any one of embodiments 37-39, wherein the result is measured at least 18 months after administration of a first therapeutically effective dose. 43. The method of any one of embodiments 37-42, wherein the subject is switched from an initiation dosing regimen to a maintenance dosing regimen.Attorney Docket No.08061.0062-00304 44. The method of embodiment 43, wherein the switch to a maintenance dose occurs after at least 6 months (e.g., 6 months, or 13 months, or 18 months) following the start of the initiation dosing regimen or after the subject has converted to amyloid negative status, e.g., as determined by an improvement in a biomarker. 45. The method of embodiment 43 or embodiment 44, wherein the initiation dosing regimen comprises an intravenous infusion at a therapeutically effective dose of 10 mg / kg relative to the weight of the subject every two weeks. 46. The method of embodiment 43 or 44, wherein the initiation dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 720 mg. 47. The method of embodiment 43 or 44, wherein the initiation dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 500 mg. 48. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises an intravenous infusion at a therapeutically effective dose of 10 mg / kg relative to the weight of the subject every month. 49. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 360 mg. 50. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 250 mg weekly. 51. The method of any one of embodiments 43-45, wherein the maintenance dosing regimen comprises the same dosing regimen as the initiation dosing regimen. 52. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is not on an anticoagulant and administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody. 53. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is not on a thrombolytic agent and administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody. 54. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is on an anticoagulant or a thrombolyticAttorney Docket No.08061.0062-00304 agent (e.g., aspirin, fibrinolytic), administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, and monitoring for ARIA in said patient. 55. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, administering an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) if needed, and monitoring the subject for ARIA. 56. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising: a. administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody; b. stopping administration of the anti-amyloid β (Aβ) protofibril antibody to the subject when administering an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) to the subject; c. resuming administration of the anti-amyloid β (Aβ) protofibril antibody to the subject at or after the time that the anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) is no longer being administered to the subject, and d. monitoring the subject for ARIA. 57. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is on an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) and delaying administration of an anti-amyloid β (Aβ) protofibril antibody to the subject until treatment with said anticoagulant or said thrombolytic agent has ended. 58. The method of any one of embodiments 1-57, wherein the subject shows a change and / or a difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment as compared to a reference measurement (e.g., measurement from a healthy control). 59. The method of embodiment 58, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, p- tau (e.g., p-tau181, p-tau217, p-tau231, the ratio of p-tau181 / np-tau181, and / or the ratio of p- tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), andAttorney Docket No.08061.0062-00304 d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, P-tau231, the ratio of P- tau181 / NP-tau181, and / or the ratio of P-tau217 / NP-tau217), glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). 60. The method of any one of embodiments 1-59, wherein the subject is amyloid-positive prior to treatment, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation, and / or a blood biomarker assessment (e.g. an Aβ1-42 / 1-40 ratio, plasma p- tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217). 61. The method of any one of embodiments 1-60, wherein the subject is ApoE4-positive. 62. The method of any one of embodiments 1-61, wherein the subject is monitored for development of ARIA. 63. The method of any one of embodiments 1-62, wherein the subject is 65 to 80 years old. 64. The method of any one of embodiments 1-62, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 65. The method of any one of embodiments 1-64, wherein the subject has Alzheimer’s disease. 66. The method of any one of embodiments 1-65, wherein the subject has early Alzheimer’s. 67. The method of any one of embodiments 1-66, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia.; b. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant;Attorney Docket No.08061.0062-00304 e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 68. The method of any one of embodiments 1-67, wherein the subject is suspected of having AD 69. The method of any one of embodiments 1-68, wherein the subject is a subject at risk for developing AD. 70. The method of embodiment 69, wherein the subject at risk for developing AD has pre- Alzheimer’s disease (pre-AD). 71. The method of embodiment 69 or embodiment 70, wherein the subject does not have cognitive impairment. 72. The method of any one of embodiments 69-71, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 73. The method of any one of embodiments 69-72, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 74. The method of any one of embodiments 69-73, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years. 75. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 76. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chainAttorney Docket No.08061.0062-00304 complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 77. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 78. A method of converting an amyloid positive subject to amyloid negative comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 79. The method of any one of embodiments 75-78, wherein the antibody subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and / or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously. 80. The method of any one of embodiments 75-79, wherein the antibody subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously. 81. The method of any one of embodiments 75-80, wherein the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg. 82. The method of any one of embodiments 75-81, wherein the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg. 83. The method of any one of embodiments 75-82, wherein the dose is administered in two parts, e.g., consecutively.Attorney Docket No.08061.0062-00304 84. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once weekly. 85. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once biweekly. 86. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once monthly. 87. The method of any one of embodiments 75-86, wherein the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen. 88. The method of embodiment 87, wherein the initiation dose is 500 mg. 89. The method of embodiment 87 or embodiment 88, wherein the initiation dose is greater than the maintenance dose. 90. The method of any one of embodiments 87-89, wherein the maintenance dose is 360 mg. 91. The method of any one of embodiments 87-90, wherein the maintenance dose is 250 mg. 92. The method of any one of embodiments 87-91, wherein the initiation dose is administered weekly. 93. The method of any one of embodiments 87-92, wherein the maintenance dose is administered weekly. 94. The method of any one of embodiments 87-92, wherein the maintenance dose is administered biweekly. 95. The method of any one of embodiments 87-94, wherein the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months. 96. The method of embodiment 95, wherein the first time period is at least 18 months. 97. The method of embodiment 95 or embodiment 96, wherein the first time period is at least 24 months. 98. The method of any one of embodiments 87-97, wherein the first time period lasts until the subject is amyloid negative. 99. The method of any one of embodiments 87-98, wherein the anti-protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months, and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time.Attorney Docket No.08061.0062-00304 100. The method of any one of embodiments 87-98, wherein the anti-protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months, and then subcutaneously administered at a maintenance dose of 360 mg biweekly for the second period of time. 101. The method of any one of embodiments 87-100, wherein the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression. 102. The method of any one of embodiments 87-101, wherein the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject. 103. The method of any one of embodiments 87-102, wherein the maintenance dose is subcutaneously administered with an autoinjector (AI). 104. The method of any one of embodiments 75-103, wherein the anti-Aβ protofibril antibody is administered subcutaneously to the subject after intravenous administration of the antibody. 105. The method of any one of embodiments 75-103, wherein the anti-Aβ protofibril antibody is administered subcutaneously to the subject prior to intravenous administration of the antibody. 106. The method of embodiment 104 or embodiment 105, wherein the intravenous infusion is 10 mg / kg relative to the weight of the subject, administered biweekly. 107. The method according to any one of embodiments 75-106, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe. 108. The method according to any one of embodiments 75-106, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in an autoinjector. 109. The method according to any one of embodiments 75-108, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 110. The method according to any one of embodiments 75-108, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 111. The method of any one of embodiments 75-110, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 112. The method of embodiment 111, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32),Attorney Docket No.08061.0062-00304 b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42 / 1-40 and / or increased total tau, p- tau (e.g., p-tau181, p-tau217, and / or p-tau231), the ratio of p-tau181 / np-tau181, and / or the ratio of p- tau217 / np-tau217, neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). 113. The method of any one of embodiments 75-112, wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation, and / or a blood biomarker assessment (e.g. a plasma Aβ1-42 / 1-40 ratio, plasma p-tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217). 114. The method according to any one of embodiments 75-113, wherein the subject is ApoE4- positive. 115. The method of any one of embodiments 75-114, wherein the subject is monitored for development of ARIA. 116. The method any one of embodiments 75-115, wherein the subject is 65 to 80 years old. 117. The method any one of embodiments 75-115, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 118. The method of any one of embodiments 75-117, wherein the subject has Alzheimer’s disease. 119. The method of any one of embodiments 75-118, wherein the subject has early Alzheimer’s disease. 120. The method of any one of embodiments 75-119, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia;Attorney Docket No.08061.0062-00304 b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 121. The method of any one of embodiments 75-117, wherein the subject is suspected of having AD. 122. The method of any one of embodiments 75-117, wherein the subject is a subject at risk for developing AD. 123. The method of embodiment 122, wherein the subject at risk for developing AD has pre-AD. 124. The method of embodiment 123 or embodiment 124, wherein the subject does not have cognitive impairment. 125. The method of any one of embodiments 122-124, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 126. The method of any one of embodiments 122-125, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 127. The method of any one of embodiments 122-126, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 128. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3)Attorney Docket No.08061.0062-00304 comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 129. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 130. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 131. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determiningAttorney Docket No.08061.0062-00304 regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 132. The method of any one of embodiments 128-131, wherein the maintenance dose is 500 mg. 133. The method of any one of embodiments 128-131, wherein the maintenance dose is 360 mg. 134. The method of any one of embodiments 128-131, wherein the maintenance dose is 250 mg. 135. The method of any one of embodiments 128-134, wherein the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 136. The method of any one of embodiments 128-135, wherein the initiation dose of the antibody is administered intravenously for at least 18 months. 137. The method of any one of embodiments 128-136, wherein the initiation dose of the antibody is administered intravenously for at least 24 months. 138. The method of any one of embodiments 128-137, wherein the maintenance dose of the antibody is administered weekly. 139. The method of any one of embodiments 128-137, wherein the maintenance dose of the antibody is administered biweekly. 140. The method of any one of embodiments 128-139, wherein the maintenance dose of the antibody is administered using a vial-syringe. 141. The method of any one of embodiments 128-139, wherein the maintenance dose of the antibody is administered using an AI. 142. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, andAttorney Docket No.08061.0062-00304 LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 143. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 144. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 145. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising:Attorney Docket No.08061.0062-00304 subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 146. The method of any one of embodiments 142-145, wherein the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 147. The method of any one of embodiments 142-146, wherein the initiation dose of the antibody is administered subcutaneously for at least 18 months. 148. The method of any one of embodiments 142-147, wherein the initiation dose of the antibody is administered subcutaneously for at least 24 months. 149. The method of any one of embodiments 142-148, wherein the initiation dose of the antibody is administered using a vial-syringe. 150. The method of any one of embodiments 142-148, wherein the initiation dose of the antibody is administered using an AI. 151. The method of any one of embodiments 142-150, wherein the maintenance dose of the antibody is administered weekly. 152. The method of any one of embodiments 142-150, wherein the maintenance dose of the antibody is administered biweekly. 153. The method of any one of embodiments 142-152, wherein the maintenance dose of the antibody is administered using a vial-syringe. 154. The method of any one of embodiments 142-152, wherein the maintenance dose of the antibody is administered using an AI. 155. The method according to any one of embodiments 128-154, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 156. The method according to any one of embodiments 128-155, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 157. The method of any one of embodiments 128-156, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 158. The method of embodiment 157, wherein the change in the measurement is selected from:Attorney Docket No.08061.0062-00304 a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42 / 1-40, and / or increased total tau, p- tau (e.g, p-tau181, p-tau217, and / or p-tau231), ratio of p-tau181 / np-tau181, ratio of p-tau217 / np- tau217, neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231, ratio of p- tau181 / np-tau181, ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL). 159. The method of any one of embodiments 128-158 wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation. 160. The method according to any one of embodiments 128-159, wherein the subject is ApoE4- positive. 161. The method of any one of embodiments 128-160, wherein the subject is monitored for development of ARIA. 162. The method any one of embodiments 128-161, wherein the subject is 65 to 80 years old. 163. The method any one of embodiments 128-161, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 164. The method of any one of embodiments 128-163, wherein the subject has Alzheimer’s disease. 165. The method of any one of embodiments 128-164, wherein the subject has early Alzheimer’s disease. 166. The method of any one of embodiments 128-165, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia;Attorney Docket No.08061.0062-00304 b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 167. The method of any one of embodiments 128-166, wherein the subject is suspected of having AD. 168. The method of any one of embodiments 128-163, wherein the subject is a subject at risk for developing AD. 169. The method of embodiment 168, wherein the subject at risk for developing AD has pre-AD. 170. The method of any one of embodiments 168 or embodiment 169, wherein the subject does not have cognitive impairment. 171. The method of any one of embodiments 168-170, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 172. The method of any one of embodiments 168-171, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 173. The method of any one of embodiments 168-172, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 174. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprisingAttorney Docket No.08061.0062-00304 amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg / kg relative to the weight of the subject. 175. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg / kg relative to the weight of the subject. 176. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg / kg relative to the weight of the subject. 177. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determiningAttorney Docket No.08061.0062-00304 regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and intravenously administering, e.g., after 18 months at the initiation dose, the antibody monthly at a dose of 10 mg / kg relative to the weight of the subject. 178. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 179. A method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg.Attorney Docket No.08061.0062-00304 180. A method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 181. A method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 182. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprisingAttorney Docket No.08061.0062-00304 amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 183. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 500 mg. 184. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 360 mg. 185. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 250 mg. 186. The method of any one of embodiments 178-185, wherein the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe. 187. The method of any one of embodiments 178-185, wherein the subcutaneously administered maintenance dose of the antibody is administered using an AI. 188. The method of any one of embodiments 178-187, wherein the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab. 189. The method of embodiment 188, wherein the first anti-Aβ antibody is donanemab. 190. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly at a dose of 360 mg. 191. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising threeAttorney Docket No.08061.0062-00304 heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg / kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 360 or 250 mg. BRIEF DESCRIPTION OF DRAWINGS Figure 1 shows the results for CDR-SB, ADAS-cog14, and ADCS MCI-ADL in Study 301. Figure 2 shows the adjusted mean change from baseline in CDR-SB in Study 301. Figure 3 shows the adjusted mean change from baseline in ADAS-Cog14 in Study 301. Figure 4 shows the adjusted mean change from baseline in ADCS MCI-ADL in Study 301. Figure 5 shows the reduction in brain amyloid beta plaque (adjusted mean change from baseline in amyloid beta PET centiloids) in Study 301. Figure 6 shows the health-related quality of life measures EQ-5D-5L (Health Today Subject). Figure 7 shows the health-related quality of life measures QOL-AD (Total Score Subject). Figure 8 shows the health-related quality of life measures QOL-AD (Subject by Proxy). Figure 9 shows the health-related quality of life measures Zarit Burden Interview – Study Partner Burden (Total Score). Figure 10 shows the time to worsening of global CDR scores. Figure 11 shows the slope analysis using CDR-SB: observed data and extrapolation to 2 Years. Figure 12 shows the change in plasma GFAP by treatment.Attorney Docket No.08061.0062-00304 Figure 13 shows ARIA rates and antithrombotic use in the Clarity AD double-blind core period. Figure 14 shows ARIA rates and antithrombotic use by genotype in the Clarity AD double-blind core period. Figure 15 shows ARIA rates and antithrombotic use in Clarity AD Core and OLE. Figure 16 shows ARIA rates and antithrombotic use by genotype in Clarity AD Core and OLE. Figure 17 shows expected ARIA-E rates for autoinjector and IV. Figure 18 shows average steady-state concentrations for routes of administration. Figure 19 shows baseline clinical characteristics of Study 301. Figure 20 shows results for primary and key secondary endpoints from Study 301. Figure 21 shows the overall safety profile from Study 301. Figure 22 shows ARIA and infusion-related reaction differences from placebo in Study 301. Figure 23 shows infusion-related reaction grades and timing in treatment in Study 301. Figure 24 shows ARIA-E events in 897 subjects who received a placebo and 898 subjects who received leacanemab. Figure 25 shows that ~90% of ARIA-E cases occurred after ≤ 6 months of treatment, and resolved within 4 months of detection. Figure 25A shows the probability of ARIA-E occurrence from 0-76 weeks. Figure 25B shows the probability of ARIA-E occurrence from 0-120 weeks. Figure 26 shows that isolated ARIA-H (without ARIA-E) occurred at a similar rate between lecanemab and placebo in Study 301. Figure 27 shows that most ARIA-H events were microhemorrhages and superficial siderosis in conjunction with ARIA-E in Study 301. Figure 28 shows that rates of ARIA were not increased with concurrent antiplatelet or anticoagulant use relative to lecanemab alone. Figure 29 shows event rates of ARIA, ARIA-E and ARIA-H based on APOE4 carrier status. Figure 30 shows a summary of ARIA case by number of microhemorrhages at baseline, by APOE4 status.Attorney Docket No.08061.0062-00304 Figure 31 shows a concentration-time profile of lecanemab following single intravenous (10 mg / kg; n=30) and subcutaneous (700 mg; n=29) doses. Figure 32 shows a concentration-time profile of lecanemab following a single subcutaneous (700 mg) dose in Japanese (n=5) versus non Japanese subjects (n=24) Figure 33 shows the mean (SD) serum concentration-time curves of lecanemab, presented on a linear and semi-logarithmic scale, comparing subcutaneous administration from a vial / syringe and via an AI device. Figure 34 shows boxplots for Cmaxof lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial / Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 35 shows boxplots for AUC(0-inf) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial / Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 36 shows boxplots for AUC(0-t) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial / Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 37 shows an overview of the study design for Study 301, including the Core Study, Extension Study, and Subcutaneous Substudies. Figure 38 shows the effect of body weight on model predicted lecanemab exposure (and their ratio) following fixed 720 mg weekly SC (vial / syringe) and 10 mg / kg biweekly IV dosing. Figure 39 shows a comparison of average steady-state concentration following 10 mg / kg biweekly IV (Study 301 Core and OLE) or 720 mg SC AI Weekly (Study 301 OLE AI Substudy). Figure 40 shows simulated lecanemab average steady-state concentrations (Cave,ss) for SC 500 mg QW administered using 2 AI devices and model-predicted (observed) Cave,ssfor IV LEC10- BW in Study 301 core and OLE phase. Figure 41 shows a model projected median (90% prediction interval) amyloid PET following either 10 mg / kg IV biweekly or 500 mg SC AI weekly lecanemab. Figure 42 shows a model projected mean (90% prediction interval) change in CDR-SB following either 10 mg / kg IV biweekly or 500 mg SC AI weekly lecanemab. Figure 43 shows a projected change in amyloid PET for subjects receiving 10 mg / kg IV for 18 or 24 Months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg / kg IV Lecanemab.Attorney Docket No.08061.0062-00304 Figure 44 shows a projected change in CDR-SB for subjects receiving 10 mg / kg IV for 18 or 24 months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg / kg IV lecanemab. Figure 45 shows simulated amyloid PET profiles for IV LEC10-BW dosing over 4 years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 46 shows simulated CDR-SB profiles for IV LEC10-BW dosing for 4 years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 47 shows model-predicted plasma Aβ42 / 40 ratio and p-tau181 after various dosing regimens. AI = autoinjector, BW = biweekly, CI = Confidence Intervals, QW = weekly, Q4W = every 4 weeks. Solid line and shaded area show predicted median and 95% CI, respectively. P-tau181 = human tau protein phosphorylated at threonine in position 181. Figure 48 shows SC exposures in healthy volunteers (Study 005) and Study 301 OLE AI device substudy (AD subjects) compared to IV LEC10-BW. AD = Alzheimer’s disease; HV = healthy volunteers; IV = intravenous; n=168 with both IV and AD device. Figure 49 shows SC exposures following 360 mg QW AI maintenance doses are within the range of LEC10-BW. Figure 50 shows a Kaplan-Meier (KM) plot of actual duration for time to event. DETAILED DESCRIPTION The “amyloid hypothesis” proposes that amyloid β (Aβ) peptides play a central role in the pathogenesis of AD. Specifically, it is hypothesized that neurodegeneration in AD may be caused by deposition of Aβ plaques in brain tissue due to an imbalance between Aβ production and Aβ clearance, leading to formation of neurofibrillary tangles containing tau protein. Aβ peptides generally exist in a dynamic continuum of conformational states such that species tend to progress from monomeric Aβ, to soluble Aβ assemblies that include a range of low molecular weight oligomers to higher molecular weight protofibrils, and finally to insoluble fibrils (plaques). Targeting these soluble and insoluble Aβ tangles and plaques may provide therapeutic benefit.Attorney Docket No.08061.0062-00304 A number of immunotherapies have been developed with the intent to reduce the amount of insoluble Aβ fibrils deposited in the brain. However, a simple correlation between the quantity and progressive accumulation of insoluble amyloid plaques and the clinical course of AD has not been determined. While therapeutic strategies continue to focus on removal of insoluble amyloid plaques, an additional approach to therapy may include reducing the toxic Aβ aggregates, such as protofibrils, that may contribute to the neuronal degeneration characteristic of AD. (See, e.g., Dodort, J.-C. and May, P., “Overview on rodent models of Alzheimer’s disease.” Curr. Protocols Neurosci.2005; 9.22- 1-9.22-6; Englund, H. et al., “Sensitive ELISA detection of amyloid-β protofibrils in biological samples.” J. Neurochem.2007; 103:334-45; and Gotz, J. et al., “Transgenic animal models of Alzheimer’s disease and related disorders: histopathology, behavior and therapy.” Mol. Psychiat. 2004; 9:664-83.) In various embodiments, anti-Aβ protofibril antibodies, such as BAN2401 and other anti- Aβ protofibril antibodies, may be used to treat AD, e.g., by slowing AD progression in subjects, e.g., those at early stages of the disease when amyloid has been deposited in the brain but where the downstream neurodegenerative cascade thought to be triggered by the amyloid deposition is still relatively early in its course (i.e., limited brain tissue loss has been produced and associated clinical deficits are at a minimum). In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, and / or wherein the patient is not an ApoE4 carrier, prior to treatment. In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient has not exhibited a change, e.g., a decrease, in brain white matter at the time of treatment. In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient is not on an anticoagulant at the time of treatment, not on a thrombolytic agent, and / or wherein the patient is not an ApoE4 carrier. In various embodiments, methods are disclosed herein for treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease, wherein the patient is at a lower risk of developing ARIA based on brain imaging. In some embodiments, a patient that does not have a brain hemorrhage, e.g., a microhemorrhage or intracerebral hemorrhage, on baseline imaging is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that has had a brain hemorrhage, e.g., a microhemorrhage or intracerebral hemorrhage, onAttorney Docket No.08061.0062-00304 baseline imaging is not administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that does not exhibit a change, e.g., a decrease, in brain white matter as measured by brain imaging prior to treatment is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that exhibits a change, e.g., a decrease, in brain white matter as measured by brain imaging is not administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In various embodiments, methods are disclosed herein for selecting and treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease, wherein the patient is at a lower risk of developing ARIA, e.g., based on the use of anticoagulants or thrombolytic agents. In some embodiments, a patient receiving aspirin is administered a therapeutically effective dose of an anti- amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving an antiplatelet medication is administered a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving a thrombolytic and / or anticoagulant agent is administered a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving an anticoagulant is not selected for treatment with an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving a thrombolytic agent is not selected for treatment with an anti- amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In various embodiments, methods are disclosed herein for treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease wherein the patient is at an increased risk of an ARIA event or brain hemorrhage, e.g., a microhemorrhage, a intracerebral hemorrhage, wherein the patient is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401) and is further administered a steroid. In some embodiments, a patient receiving an anti-amyloid β (Aβ) protofibril antibody and has a severe ARIA event is administered a steroid. In some embodiments, additional patient demographics, such as age and if the subject is a carrier of the apolipoprotein E ε4 gene allele, may be used to select a patient for treatment in combination with baseline status of brain hemorrhage, e.g., presence or absence of microhemorrhage or intracerebral hemorrhage, baseline status of brain white matter, and / or treatment with an anticoagulant or thrombolytic agent, and / or additional biomarkers indicating amyloid positivity (e.g. West et al, Mol Neurodegen (2021) 16-30, Jansen et al, JAMA (2015) 1924-1938, Ossenkoppele et al, JAMA (2015) 1939-1950). In some embodiments, one or more additional biomarkers, e.g., one or more blood biomarkers (such as the ratio of Aβ 42 to Aβ 40 and / or a p-tau181) may be used to select a patient, e.g., in conjunction with brain measurements such as an amyloid or tau PET measurement. In someAttorney Docket No.08061.0062-00304 embodiments, biomarkers associated with AD pathology include (but are not limited to) one or more of: ^ amyloid in the brain (e.g., as measured by amyloid positron emission tomography (PET); ^ tau in the brain (e.g., as measured by tau PET; ^ cerebrospinal fluid (CSF) biomarkers, e.g., CSF levels of Aβ42, Aβ40, Aβ42 / Aβ40 ratio, total tau, p-tau (e.g., p-tau181, p-tau217, p-tau231), p-tau181 / np-tau181 ratio, p-tau217 / np-tau217 ratio; neurogranin; neurofilament light chain (NfL), and / or glial fibrillary acidic protein (GFAP); ^ blood biomarkers, e.g., plasma and / or serum levels of Aβ42, Aβ40, Aβ42 / Aβ40 ratio, total tau, p-tau (e.g., p-tau181, p-tau217, p-tau231), p-tau181 / np-tau181 ratio, p-tau217 / np-tau217 ratio; neurogranin; neurofilament light chain (NfL), and / or glial fibrillary acidic protein (GFAP); ^ biomarkers in other bodily fluids (e.g., urine, saliva, tears, sweat, etc.); ^ genetic biomarkers (e.g., ApoE4, PSEN1, and / or PSEN2); ^ abnormalities in eye and / or retinal vasculature (e.g., as measured by optical coherence tomography (OCT) or optical coherence tomography angiography (OCTA); and / or abnormalities in brain structure, function, and / or vasculature (e.g., as measured by magnetic resonance imaging (MRI), electroencephalograms (EEG), and / or single-photo emission computed tomography (SPECT). In some embodiments, an age and / or apolipoprotein E ε4 gene allele normalized measurement of tau PET and / or the at least one additional biomarker from a subject is used to evaluate whether a sample (e.g., a plasma sample) from a subject indicates that the subject is suitable for treatment with a protofibril antibody such as BAN2401 (e.g., if the subject is amyloid positive) and / or to monitor treatment. For example, in some embodiments, a patient who is a carrier of an apolipoprotein E ε4 gene allele may be considered amyloid positive at a lower level of a biomarker than needed to indicate amyloid positivity in a subject who is not a carrier. In some embodiments, a patient who is a carrier of an apolipoprotein E ε4 gene allele may be at a higher risk of developing ARIA in response to a treatment with an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401), than a subject who is not a carrier and, e.g., may be cautioned by a doctor of increased risk, monitored for ARIA, and / or advised not to take an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). Likewise, in another example, an older subject may be considered amyloid positive at a lower biomarker level than the level required to indicate positivity in a younger subject. In some embodiments, biomarker level is used in a Receiver Operating Characteristic (ROC) analysis to predict amyloid positivity. In some embodiments, additional patient demographics, such as age and if the subject is a carrier of an apolipoprotein E ε4 gene allele, may be used with a biomarker level in anAttorney Docket No.08061.0062-00304 ROC analysis to predict amyloid positivity. In some embodiments, the prediction of amyloid positivity in a patient is used to determine the dosage or frequency of treatment. Cognitive and functional decline can be measured by techniques known in the art, including scoring methods such as CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI-ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered in a therapeutically effective amount to reduce or delay cognitive decline. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered as a therapeutically effective dose comprising an intravenous infusion of 10 mg / kg relative to the weight of the subject. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered as a therapeutically effective dose comprising a subcutaneous administration of 720 mg. In some embodiments, the method results in less cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method results in at least 24% less (e.g., at least 29% less) cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by CDR-SB compared to an untreated subject. In some embodiments, the method results in at least 26% less (e.g., at least 27% less) cognitive decline as measured by CDR-SB compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in at least 26% less (e.g., at least 47% less) cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in at least 37% less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in a reduced risk of progression to a subsequent stage of AD as measured by a CDR global score, e.g., a higher score on a subsequent evaluation indicating progression to the next stage of AD, e.g., an unchanged score indicating remaining in the same stage of AD. In some embodiments, the result is measured at least 6 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 12 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 13 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 18 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. An anti-Aβ protofibril antibody, such as BAN2401, may be formulated in a pharmaceutical composition as disclosed in PCT / IB2021 / 000155 (WO2021 / 186245), which isAttorney Docket No.08061.0062-00304 incorporated herein by reference. In some embodiments, the composition comprises 80 mg / mL to 120 mg / mL BAN2401, 240 mM to 360 mM arginine, 0.03% w / v to 0.08% w / v polysorbate 80, and 30 mM to 70 mM citrate buffer. In some embodiments, the arginine is arginine, arginine hydrochloride, or a combination thereof. In some embodiments, the composition comprises a liquid dosage form comprising 100 mg / mL BAN2401, 50 mmol / L citrate, 350 mmol / L arginine, and 0.05% polysorbate 80. In some embodiments, the composition comprises 80 mg / mL to 240 mg / mL BAN2401, 140 mM to 260 mM arginine hydrochloride, 0.01% w / v to 0.1% w / v polysorbate 80, and 15 mM to 35 mM histidine buffer. In some embodiments, the composition comprises a liquid dosage form comprising 100 mg / mL BAN2401, 25 mmol / L histidine, 200 mmol / L arginine, and 0.05% polysorbate 80. In some embodiments, BAN2401, is formulated as disclosed in PCT / IB2021 / 000155 (WO2021 / 186245), which is incorporated herein by reference. In some embodiments, the composition comprises 80 mg / mL to 240 mg / mL BAN2401, 140 mM to 260 mM arginine hydrochloride, 0.01% w / v to 0.1% w / v polysorbate 80, and 15 mM to 35 mM histidine buffer. In some embodiments, the composition comprises a liquid dosage form comprising 200 mg / mL BAN2401, 25 mmol / L histidine, 200 mmol / L arginine, and 0.05% polysorbate 80. In some embodiments, provided herein is a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody until a desired improvement in one or more biomarkers is achieved, e.g. until an increase in the ratio of Aβ1-42 to Aβ1-40 in a fluid sample, e.g., a blood sample is observed and / or a decrease in the level of p-tau181 in a fluid sample, e.g., a blood sample is observed. In some embodiments, treatment is continued until a tau PET level has improved relative to an untreated control subject and / or treatment is continued until the ratio of Aβ1-42 to Aβ1-40 in a fluid sample, e.g., a blood sample is at or above 0.092. In some embodiments, treatment is continued until an amyloid PET or tau PET level has improved relative to an untreated control subject. In some embodiments, treatment is continued until a tau PET level has improved relative to an untreated control subject and / or the florbetapir amyloid PET SUVr negativity is below 1.17. In some embodiments, the one or more biomarkers comprises a serum or plasma GFAP measurement. In some embodiments, treatment is continued until a subject is amyloid negative. In some embodiments, a subject will switch to a maintenance dose after a desired improvement in one or more biomarkers is achieved. In some embodiments, a maintenance dosing regimen may further comprise one or more additional treatments in addition to an anti-Aβ protofibril antibody, e.g., it may comprise administering E2814. In some embodiments, provided herein is a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody until a desired improvement in the cognitive outcomes in a subject, e.g., one having Alzheimer’s disease, Pre-AD, or early Alzheimer’s disease, or other treatment outcome measures is achieved. In some embodiments, the method ofAttorney Docket No.08061.0062-00304 treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody for at least 18 months or e.g., until a desired improvement in the cognitive outcomes in a subject is achieved. Cognitive and functional decline can be measured by techniques known in the art, including scoring methods such as CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI-ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody continues until the method results in less cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the efficacy of a method of treatment may be evaluated using a CDR global score, wherein a CDR global score may be used to determine if a patient has progressed or maintained a stage of AD during treatment, e.g., a higher score on a subsequent evaluation indicating progression of AD, e.g., an unchanged score indicating no progression of AD. In some embodiments, the method of treatment continues until the method results in at least 24% less (e.g., at least 29% less) cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in less cognitive decline as measured by CDR- SB compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in at least 26% less (e.g., at least 27% less) cognitive decline as measured by CDR- SB compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in less cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in at least 26% less (e.g., at least 47% less) cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in at least 37% less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the result is measured at least 6 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 12 months after administering a therapeutically effective amount of at least one anti- Aβ protofibril antibody. In some embodiments, the result is measured at least 13 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 18 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. Methods of treatment, including dosing, by an intravenous administration of an anti-Aβ protofibril antibody are disclosed in PCT / US2022 / 073576 and PCT / US2022 / 079571 and are incorporated herein by reference. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg / kg (e.g., administering BAN2401 at 10Attorney Docket No.08061.0062-00304 mg / kg), biweekly, e.g., for at least 18 months or e.g., until a patient is amyloid-negative. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg / kg (e.g., administering BAN2401 at 10 mg / kg), biweekly, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a maintenance dose. In some embodiments, the maintenance dose may be the same as the treatment dose, or it may involve a reduced dosage and / or frequency of administration. Methods of treatment, including dosing, by a subcutaneously administered anti-Aβ protofibril antibody are disclosed in PCT / US2022 / 073576; PCT / US2022 / 079571; and PCT / US2022 / 041926 and are incorporated herein by reference. In some embodiments, a treatment comprises subcutaneously administering an anti-Aβ protofibril antibody (e.g., administering BAN2401 at 720 mg), weekly, e.g., for at least 18 months or e.g., until a patient is amyloid negative. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation, e.g., until a patient is amyloid-negative or e.g., for at least 18 months. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation, e.g., until a patient is amyloid-negative or e.g., for at least 18 months. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a weekly, subcutaneous maintenance dose, e.g., a dose of 360 mg. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a biweekly subcutaneous maintenance dose, e.g., a dose of 720 mg. In some embodiments, the method of treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation, e.g., for at least 18 months. In some embodiments, the method of treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation, e.g., for at least 18 months, before switching to a maintenance dose. In some embodiments, the maintenance dose may be the same as the treatment dose, or it may involve a reduced dosage and / or frequency of administration. In some embodiments, the method of treatment comprises using a biomarker level, to determine switching to a maintenance intravenous or subcutaneous dose at a set time point (e.g., after 18 months). In some embodiments, a maintenance dose is administered subcutaneously (e.g., as one or more subcutaneous injections). In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10Attorney Docket No.08061.0062-00304 mg / kg (e.g., administering BAN2401 at 10 mg / kg), biweekly, before switching to a subcutaneous maintenance dose, e.g., a weekly subcutaneous maintenance dose, e.g., at 720 mg. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg / kg biweekly before switching to a biweekly, 720 mg, subcutaneous maintenance dose. In some embodiments, the method of treatment comprises using a biomarker level to determine switching from a subcutaneous treatment to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering an anti-Aβ protofibril antibody, e.g., BAN2401, before switching to an intravenous maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) before switching to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg before switching to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly before switching to an intravenous maintenance dose of 10 mg / kg biweekly. In some embodiments, a subject’s maintenance dose is administered at the same amount and / or frequency as the dose during the treatment period. In some embodiments, a subject’s maintenance dose is 50% of the dose during the treatment period. In some embodiments, a patient starts on an intravenous maintenance dose, e.g., a dosing of 10 mg / kg BAN2401 as disclosed above before switching to a subcutaneous maintenance dose, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation. In some embodiments, a patient starts on a subcutaneous maintenance dose, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation before switching to an intravenous maintenance dose, e.g., a dosing of 10 mg / kg BAN2401 as disclosed above. In some embodiments, a patient is moved back from a maintenance dose to the initial treatment dose if the patient is determined to no longer be amyloid negative, e.g., as assessed by blood, serum, or CSF biomarker and / or as determined by amyloid PET SUVr. In some embodiments, a subject’s maintenance dose is administered at the same amount and / or frequency as the dose during the treatment period. In some embodiments, a subject’s maintenance dose is 50% of the dose during the treatment period. In some embodiments, the maintenance dose comprises two or more dosings, in which a first dosing is selected from the maintenance dose as exemplified above and a second and / or subsequent dosing comprising a lower amount and / or frequency of dosing than the first or previous dosing, respectively. In some embodiments, the switching to the second or subsequent dosing is determined based on one or moreAttorney Docket No.08061.0062-00304 biomarkers as exemplified above, where the levels of the biomarkers are different from (e.g., improved over) the levels used in switching from initial dose to the first dosing in the maintenance dose. In some embodiments, a patient’s treatment is discontinued if a patient no longer has early AD, e.g., as assessed by cognitive evaluation, PET SUVr, and / or blood, CSF, or plasma biomarkers. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as volumetric MRI (vMRI), comprising whole brain volume, cortical thickness, and / or total hippocampal volume. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a PET level, comprising an amyloid PET level and / or a fluorodeoxyglucose (FDG) PET level. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a cerebrospinal fluid level of a biomarker comprising the CSF level of Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, p-tau (e.g, p-tau181, p-tau217, and / or p-tau231), the ratio of p-tau181 / np- tau181, the ratio of p-tau217 / np-tau217), neurogranin, and / or neurofilament light (NfL) peptide. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a serum or plasma level of a biomarker comprising Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, phosphorylated tau (P-tau) (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and / or 231 (P-tau231), the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light (NfL). In some embodiments, a patient’s biomarkers may be monitored at least once after the discontinuation of treatment. In some embodiments, a patient’s biomarkers are monitored at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, treatment is reinitiated if a patient’s biomarker level becomes less favorable, e.g., a tau PET level increases at the same rate as an untreated control. In some embodiments, the subject has been diagnosed with early AD. In some embodiments, the subject has been diagnosed as having mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia. Methods of treatment using an anti-Aβ protofibril antibody, including a therapeutically effective dosage, are disclosed in PCT / US2022 / 073576; PCT / US2022 / 079571; and PCT / US2022 / 041926, which is herein incorporated by reference. In some embodiments, the method of treatment comprises using a biomarker level, e.g., a tau PET level or a rate of change in a tau PETAttorney Docket No.08061.0062-00304 level, to allow for monitoring and treatment decisions, e.g., altering a dosage of BAN2401 and / or discontinuing treatment. 1. Definitions The following are definitions of terms used in the present application. As used herein, the singular terms “a,” “an,” and “the” include the plural reference unless the context clearly indicates otherwise. The phrase “and / or,” as used herein, means “either or both” of the elements so conjoined, i.e., elements that are conjunctively present in some cases and disjunctively present in other cases. Thus, as a non-limiting example, “A and / or B”, when used in conjunction with open-ended language such as “comprising” can refer, in some embodiments, to A only (optionally including elements other than B); in other embodiments, to B only (optionally including elements other than A); in yet other embodiments, to both A and B (optionally including other elements); etc. As used herein, “at least one” means one or more of the elements in the list of elements, but not necessarily including at least one of each and every element specifically listed within the list of elements and not excluding any combinations of elements in the list of elements. This definition also allows that elements may optionally be present other than the elements specifically identified within the list of elements to which the phrase “at least one” refers, whether related or unrelated to those elements specifically identified. Thus, as a non-limiting example, “at least one of A and B” (or, equivalently, “at least one of A or B,” or, equivalently “at least one of A and / or B”) can refer, in one embodiment, to at least one, optionally including more than one, A, with no B present (and optionally including elements other than B); in another embodiment, to at least one, optionally including more than one, B, with no A present (and optionally including elements other than A); in yet another embodiment, to at least one, optionally including more than one, A, and at least one, optionally including more than one, B (and optionally including other elements); etc. As used herein, “about” when used in connection with doses, amounts, or ratios, include the value of a specified dose, amount, or ratio or a range of the dose, amount, or ratio that is recognized by one of ordinary skill in the art to provide a therapeutic effect equivalent to that obtained from the specified dose, amount, or ratio. The term “about” may refer to an acceptable error for a particular value as determined by one of skill in the art, which depends in part on how the values is measured or determined. In some embodiments, the term “about” means within 5% of a given value or range. When a number is recited, either alone or as part of a numerical range, it should be understood that the numerical value can vary above and below the stated value by up to a variance of + / - 10% of the stated value.Attorney Docket No.08061.0062-00304 When a range of values is listed herein, it is intended to encompass each value and sub- range within that range. For example, “2.5 mg / kg to 10 mg / kg” is intended to encompass, for example, 2.5 mg / kg, 3 mg / kg, 3.5 mg / kg, 4 mg / kg, 4.5 mg / kg, 5 mg / kg, 5.5 mg / kg, 6 mg / kg, 6.5 mg / kg, 7 mg / kg, 7.5 mg / kg, 8 mg / kg, 8.5 mg / kg, 9 mg / kg, 9.5 mg / kg, 10 mg / kg, 2.5 mg / kg to 3 mg / kg, 2.5 mg / kg to 4.5 mg / kg, 3 mg / kg to 4.5 mg / kg, 4.5 mg / kg to 8 mg / kg, 2.5 mg / kg to 9 mg / kg, and so forth. As used herein, “adjusted mean change from baseline” refers to the use of a statistical analysis to calculate the change in a biomarker value over time. In some embodiments, a linear mixed-effects model (MMRM) is used to account for at least one additional covariate to determine the adjusted mean change from baseline. As used herein, “baseline” refers to an initial measurement (e.g., a measure of cognitive function, a brain structure, amyloid burden, and / or a fluid biomarker) taken at a first or an early time point and used for comparison over time to evaluate changes in the measurement. A change in a measurement over time as compared to a baseline may be used to assess the progression of a disease and / or the effect of a treatment for the disease. Amyloid β 1-42 (Aβ42) refers to an amyloid beta monomer from amino acid 1 to 42 of the full-length protein (Table 5, SEQ ID NO:13). Amyloid β 1-40 (Aβ1-40) refers to an amyloid beta monomer from amino acid 1 to 40 of the full-length protein (Table 5, SEQ ID NO:14). P-tau181 (also p-Tau181 or p-tau181) is human tau protein phosphorylated at threonine in position 181. NP-tau181 (also np-Tau181 or np-tau181) refers to human tau which is not phosphorylated at threonine in position 181. P-Tau181 / NP-Tau181 (p-Tau181 / np-Tau181, p- tau181 / np-tau181, P-Tau181R, p-Tau181R, or p-tau181R) may refer to the ratio of tau phosphorylated at threonine in position 181 to non-phosphorylated tau at threonine in position 181. P-tau217 (also p-Tau217 or p-tau217) is human tau protein phosphorylated at threonine in position 217. NP-Tau217 (also np-Tau 217 or np-tau217) refers to human tau which is not phosphorylated at threonine in position 217. P-Tau217 / NP-Tau217 (also p-Tau217 / np-Tau217, p- tau217 / np-tau217, P-Tau217R, p-Tau217R, or p-tau217R) may refer to the ratio of tau phosphorylated at threonine in position 217 to non-phosphorylated tau at threonine in position 217. P-tau231 (also p-Tau231 or p-tau231) is human tau protein phosphorylated at threonine in position 231. NP-Tau231(also np-Tau 231or np-tau231) refers to human tau which is not phosphorylated at threonine in position 231. P-Tau231 / NP-Tau231 (also p-Tau231 / np-Tau231, p- tau231 / np-tau231, P-Tau231R, p-Tau231R, or p-tau231R) may refer to the ratio of tau phosphorylated at threonine in position 231 to non-phosphorylated tau at threonine in position 231.Attorney Docket No.08061.0062-00304 Total tau or t-tau as used herein is a measure of total tau in a sample, e.g. a CSF sample, a plasma sample, a serum sample. Patients (also called “subjects”) with “preclinical AD” or “pre-AD” as described herein, are cognitively normal individuals with intermediate or elevated levels of amyloid in the brain and can be identified by asymptomatic stages with or without memory complaints and emerging episodic memory and executive function deficits. Such patients may be identified by one or more biomarker. Cognitively normal can include individuals who are CDR 0, or individuals within the normal ranges of cognitive test scores (MMSE, International Shopping List Task, Logical Memory, etc.). Preclinical AD occurs prior to significant irreversible neurodegeneration and cognitive impairment and is typically characterized by the appearance of in vivo molecular biomarkers of AD and the absence of clinical symptoms. Preclinical AD biomarkers that may suggest the future development of Alzheimer’s disease include, but are not limited to, one or more of intermediate or elevated levels of amyloid in the brain by amyloid, fluorodeoxyglucose (FDG), or tau positron emission tomography (PET) (e.g., a centiloid measure of about 20-40, e.g., a measure of about 20-32), cerebrospinal fluid level of Aβ1-42 and / or Aβ1-42 / 1-40 ratio, cerebrospinal fluid level of total tau, cerebrospinal fluid level of p-tau (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and / or 231 (P-tau231), the ratio of P-tau181 / NP-tau181, and / or the ratio of P-tau217 / NP-tau217), cerebrospinal fluid level of neurogranin, cerebrospinal fluid level of neurofilament light peptide (NfL), and blood biomarkers as measured in the serum or plasma (e.g. levels of Aβ1-42, the ratio of two forms of amyloid-β peptide (Aβ1-42 / 1-40 ratio, e.g., a ratio of between about 0.092-0.094 or below about 0.092), plasma levels of plasma total tau (T-tau), levels of phosphorylated tau (P-tau) isoforms (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and / or 231 (P-tau231)), the ratio of P-tau181 / NP-tau181, and / or the ratio of P-tau217 / NP-tau217), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL)). For example, it has been found that subjects treated with elenbecestat (E2609), a β-site amyloid precursor protein cleaving enzyme (BACE) inhibitor, who had amyloid baseline positron emission tomography (PET) standard uptake value ratios (SUVr values) of 1.4 to 1.9, exhibited the greatest slowing of cognitive decline while on treatment. See Lynch, S. Y. et al. “Elenbecestat, a BACE inhibitor: results from a Phase 2 study in subjects with mild cognitive impairment and mild-to- moderate dementia due to Alzheimer’s disease.” Poster P4-389, Alzheimer’s Association International Conference, July 22-26, 2018, Chicago, IL, USA. Similarly, it has been found that subjects having a baseline florbetapir amyloid PET SUVr levels below 1.2 do not exhibit enough cognitive decline to be detectable, whereas subjects having SUVr levels above 1.6 appear to correlate with a plateau effect in which amyloid level has reached a saturation level and treatment does not result in a change of cognitive measures. See Dhadda, S. et al., “Baseline florbetapir amyloid PET standard update value ratio (SUVr) can predict clinical progression in prodromal Alzheimer’s diseaseAttorney Docket No.08061.0062-00304 (pAD).” Poster P4-291, Alzheimer’s Association International Conference, July 22-26, 2018, Chicago, IL, USA. “Early AD” or “early Alzheimer’s disease,” as used herein, is a continuum of AD severity from mild cognitive impairment due to AD – intermediate likelihood to mild Alzheimer’s disease dementia. Subjects with early AD include subjects with mild Alzheimer’s disease dementia as defined herein and subjects with mild cognitive impairment (MCI) due to AD – intermediate likelihood as defined herein. In some embodiments, subjects with early AD have MMSE scores of 22 to 30 and Clinical Dementia Rating (CDR) global range 0.5 to 1.0. Other methods for detecting early AD disease may employ the tests and assays specified below, including the National Institute of Aging- Alzheimer’s Association (NIA-AA) core clinical criteria for probable Alzheimer’s disease dementia in McKhann, G.M. et al., “The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging – Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease.” Alzheimer Dement.2011; 7:263-9. Other methods include CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI- ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, a subject with early AD has evidence of elevated amyloid in the brain or a positive amyloid load. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and / or confirmed by PET assessment. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and / or confirmed by a CSF assessment of markers such as Aβ1-42 (e.g., a soluble CSF biomarker analysis). In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and / or confirmed by measuring the level of p-tau181. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and / or confirmed by an MRI. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated by retinal amyloid accumulation. In some embodiments, more than one assessment method is used. “Amyloid” refers to fibers that are unbranched, usually extracellular, and found in vivo; in addition, the fibers bind the dye Congo Red and then show green birefringence when viewed between crossed polarizers. Amyloid-forming proteins have been identified and associated with serious diseases, including amyloid-β peptide (Aβ) with Alzheimer’s disease (AD), islet amyloid polypeptide (IAPP) with diabetes type 2, and prion protein (PrP) with the spongiform encephalopathies. As used herein, “amyloid,” “brain amyloid,” and “amyloid-β peptide (Aβ)” are used interchangeably. In some embodiments, the subject has “elevated amyloid” or “intermediate amyloid.” As one of ordinary skill in the art will recognize, amyloid levels from amyloid PET can be reported using the Centiloid method in “centiloid” units (CL). (Klunk WE et al. The Centiloid Project: standardizingAttorney Docket No.08061.0062-00304 quantitative amyloid plaque estimation by PET. Alzheimer’s Dement.2015; 11:1–15 e1–4). The Centiloid method measures a tracer on a scale of 0 CL to 100 CL, where 0 is deemed the anchor-point and represents the mean in young healthy controls and 100 CL represents the mean amyloid burden present in subjects with mild to moderate severity dementia due to AD. (Id.) As is known to one of ordinary skill in the art, centiloid thresholds may vary, for example may be refined, based on new or additional scientific information. (See, e.g., http: / / www.gaain.org / centiloid-project.) An elevated level of amyloid can be set relative to a baseline threshold in a healthy control determined according to methods known to a person of ordinary skill in the art (POSA). For example, a centiloid value of 32.5 can be used as a threshold value for “elevated amyloid,” and an “intermediate amyloid” level refers to an Aβ amyloid PET in the range of 20-32.5 CL (e.g., 30 CL). In another example, a centiloid value of 40 can be used as a threshold value for “elevated amyloid,” and an “intermediate amyloid” level refers to an Aβ amyloid PET in the range of 20-40 CL. Subjects with “mild Alzheimer’s disease dementia,” or “mild AD dementia” as used herein, are subjects meeting the National Institute of Aging-Alzheimer’s Association (NIA-AA) core clinical criteria for probable Alzheimer’s disease dementia in McKhann, G.M. et al., “The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging – Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease.” Alzheimer Dement.2011; 7:263-9. Also included herein are subjects who have a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater at screening and baseline and subjects that exhibit change in the score on the Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). Subjects with “MCI due to AD – intermediate likelihood,” as used herein are those identified as such in accordance with the NIA-AA core clinical criteria for mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood (see McKhann supra). For example, a subject may be symptomatic but not demented, with evidence of brain amyloid pathology making them less heterogeneous and more similar to mild Alzheimer’s disease dementia subjects in cognitive and functional decline as measured by the ADCOMS Composite Clinical Score defined herein. Also included are subjects who have a CDR score of 0.5 and a Memory Box score of 0.5 or greater at screening and baseline. Furthermore, subjects who report a history of subjective memory decline with gradual onset and slow progression over the last 1 year before screening, which is corroborated by an informant, are also included herein. Memory decline and / or episodic memory impairment can be assessed in a subject by change in the score on the Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II). As used herein, a “control subject”, “untreated AD subject”, or an “untreated control subject” is a subject that is not being treated or has been treated for Alzheimer’s disease. In some embodiments, a control subject has Alzheimer’s disease. In some embodiments, the control subjectAttorney Docket No.08061.0062-00304 has early Alzheimer’s disease, or pre-Alzheimer’s disease. In some embodiments, the control subject has Alzheimer’s disease and is not treated with an anti-Aβ protofibril antibody. The terms “patient” and “subject” are used interchangeably. As used herein, “MMSE” refers to the Mini-Mental State Examination, a cognitive instrument commonly used for screening purposes, but also often measured longitudinally in AD clinical trials having a 30 point scale with higher scores indicating less impairment and lower scores indicating more impairment, ranging from 0 (most impaired) to 30 (no impairment). In some embodiments, seven items measuring orientation to time and place, registration, recall, attention, language, and drawing may be assessed as part of the MMSE score. (Folstein, M.F. et al., “Mini- mental state. A practical method for grading the cognitive state of patients for the clinician.” J. Psychiatr. Res.1975;12:189-98.) As used herein, “ADAS-Cog” refers to Alzheimer’s Disease Assessment Scale-Cognitive. The ADAS-Cog is a widely used cognitive scale in Alzheimer's disease trials having a structured scale that evaluates memory (word recall, delayed word recall, and word recognition), reasoning (following commands), language (naming, comprehension), orientation, ideational praxis (placing letter in envelope) and constructional praxis (copying geometric designs). (Rosen, W.G. et al., “A new rating scale for Alzheimer’s disease.” Am. J. Psychiatry 1984; 141:1356-64.) Ratings of spoken language, language comprehension, word finding difficulty, ability to remember test instructions, maze, and number cancellation may also be obtained. In some embodiments, ADAS-Cog refers to the use of the Alzheimer Disease Assessment Scale-Cognitive Subscale14(ADAS-Cog14). In some embodiments, a modified version may be used herein and is scored from 0 to 90 points with a score of 0 indicating no impairment, and a score of 90 indicating maximum impairment. In some embodiments, the ADAS–Cog14 tasks include memory (word recall, delayed word recall, and word recognition), reasoning (following commands), language (naming, comprehension), orientation, ideational praxis (placing letter in envelope), constructional praxis (copying geometric designs), spoken language, language comprehension, word finding difficulty, ability to remember test instructions, maze, and number cancellation (Rosen et al, 1984). As used herein, “CDR-SB” refers to clinical dementia rating - sum of boxes. The CDR is a clinical scale that describes 5 degrees of impairment in performance on each of 6 categories of function including memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. (Berg, L. et al., “Mild senile dementia of the Alzheimer type: 2. Longitudinal assessment.” Ann. Neurol.1988; 23:477-84.) A sum of boxes score provides a measure of change where each category has a maximum possible score of 3 points and the total score is a sum of the category scores giving a total possible score of 0 to 18 with higher scores indicating more impairment.Attorney Docket No.08061.0062-00304 As used herein, “CDR global”, “global CDR” score and “global rating of dementia CDR” score is used interchangeably. As used herein, CDR global score is a rating of the degree of impairment obtained on each of the 6 categories of function from the 6 categories of the CDR scaleand is synthesized into 1 global rating of dementia CDR score, (ranging from 0 to 3) where 0 indicates no cognitive impairment, 0.5 indicates mild cognitive impairment, and 1-3 indicates mild, moderate, severe dementia respectively. The global CDR score may be used as a clinical measure of severity of dementia. In some embodiments, a global CDR score may be used to determine if a patient has progressed or maintained a stage of AD, e.g., a higher score on a subsequent evaluation indicating progression of AD, e.g., an unchanged score indicating no progression of AD. As used herein, “ADCOMS” refers to Alzheimer’s Disease Composite Score, a composite clinical score based on an analysis of four ADAS-Cog items (delayed word recall, orientation, word recognition, and word finding difficulty), two Mini Mental State Examination (MMSE) items (orientation to time, and drawing), and all six CDR-SB items (personal care, community affairs, home and hobbies, memory, orientation, and judgment and problem solving), as discussed in the Examples and in Wang, J. et al., “ADCOMS: a composite clinical outcome for prodromal Alzheimer’s disease trials.” J. Neurol. Neurosurg. Psychiatry.2016; 87:993-999. ADCOMS was developed to be particularly sensitive to disease progression during early stages of AD (i.e., preclinical AD or early AD). In some embodiments, ADCOMS can be calculated using the following formula: ^ଶ ^ ^^^^ ^^^ ൌ ^ ^^^^^^^ ^^^ ^^ ^^^^^^^ ^^^ ^^ ^^^^^^^ ^^^ where ^^^^ ^^^, ^^^^ ^^^ and ^^^^ ^^^from ADAS-cog, reversed MMSE scores, and CDR-SB, respectively (Wang, J. et al., “ADCOMS: a composite clinical outcome for prodromal Alzheimer’s disease trials). ADCOMS is particularly sensitive to disease progression during early stages of AD, i.e., prodromal and mild AD. As used herein, “ADCS MCI-ADL” refers to the Alzheimer's Disease Cooperative Study- Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS MCI-ADL). The ADCS MCI-ADL is a clinical scale that assesses the competence level of a patient at six basic activities of daily living. Additional examples are discussed in Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. As used herein, “modified iADRS” or “iADRS” refers to a composite tool that combines scores from the ADAS Cog14 (all items) and the ADCS MCI-ADL (all items). The modified iADRS score can be used to evaluate disease progression:Attorney Docket No.08061.0062-00304 Modified iADRS score = [-1(ADAS-cog14) +90] + ADCS MCI-ADL. As used herein, “ApoE4-positive” subjects and “ApoE4 carriers” refer to subjects who harbor the ε4 variant of the apolipoprotein (APOE) gene. As used herein, APOE4 status refers to a subject’s status as a gene carrier. The ε4 variant is one of several major alleles of the apolipoprotein gene. The gene is generally responsible for metabolism of fats. It has been found that carriers of the apolipoprotein ε4 show significantly greater rates of amyloid retention when compared to non- carriers. (Drzezga, A. et al, “Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease.” Neurology.2009; 72:1487-94.) In some embodiments, a subject treated herein is a heterozygous carrier of the apolipoprotein E ε4 gene allele. In some embodiments, the subject is a homozygous carrier of the apolipoprotein E ε4 gene allele. The terms “ApoE4- negative” and “ApoE4 non-carriers” are used interchangeably. As used herein, whether an early AD subject is “amyloid positive” or “amyloid negative” may be determined based on whether the subject has a positive amyloid load. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative as indicated by longitudinal positron emission tomography (PET) assessment of an imaging agent uptake into the brain, e.g., an amyloid imaging agent or a tau imaging agent. In some embodiments, a subject is determined to be amyloid- positive or amyloid-negative by evaluation of a tau PET imaging assessment. In some embodiments, a subject is “amyloid negative” if the florbetapir amyloid PET SUVr negativity is below 1.17. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative by evaluation of the level of a biomarker in a sample (e.g., a Aβ42 / 40 ratio) from a subject, alone or in combination with another method such as PET measurement of brain amyloid. In some embodiments, a subject is “amyloid negative” if the Aβ42 / 40 ratio in a sample is at or about above 0.092-0.094 e.g., at about 0.092. In some embodiments, a subject is “amyloid negative” if the Aβ42 / 40 ratio in a sample is above 0.092. In some embodiments, a subject is determined to be amyloid-positive or amyloid- negative by a CSF assessment of the presence of amyloid pathology using assessments of markers such as p-tau181, alone or in combination with another method such as PET measurement of brain amyloid. In some embodiments, a qualitative visual read of PET scans may be used to determine amyloid positive and amyloid negative by categorizing subjects as having either “normal” or “abnormal” uptake on the basis of the PET image pattern. Readers will have been trained and certified to recognize brain PET images with abnormal or normal patterns of uptake, or the detection of amyloid is done through a semi-quantitative or quantitative approach. In some embodiments, a threshold will be set for quantitatively determining from a biomarker (e.g., serum or CSF) and / or PET scan whether an Aβ brain load indicates a subject is amyloid-positive or negative. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative by an MRI. In someAttorney Docket No.08061.0062-00304 embodiments, a subject is determined to be amyloid-positive or amyloid-negative by retinal amyloid accumulation. In some embodiments, a subject is determined to be amyloid-positive or amyloid- negative by behavioral / cognitive phenotypes. As would be understood by one of ordinary skill in the art, digital, computerized, and / or conventional (e.g., pen and paper) cognitive tests may be used to detect early cognitive changes that may signal mild cognitive impairment and / or a risk for developing dementia, and thus may be used to identify subject in need of treatment as disclosed herein. Such tests, for example, may screen for cognitive impairment, and potentially identify individuals with MCI. Tests may use artificial intelligence to analyze cognitive test results to determine whether a case of mild cognitive impairment will escalate into Alzheimer’s within a year. Diagnosing the condition early, before symptoms have begun to appear, may be used to assist physicians identify subjects in need of treatment as disclosed herein sooner, potentially delaying onset or lessening the severity of the neurodegenerative disease. As used herein, the term “treat” refers to any administration or application of a therapeutic agent for a disease or disorder in a subject, and includes inhibiting the disease, slowing progression of the disease, delaying progression, arresting its development, reversing progression of disease (e.g., reversing build up of Aβ fibrils), preventing the onset or development of the disease, relieving or ameliorating one or more symptoms or underlying condition(s) of the disease, curing the disease, improving one or more clinical metrics, or preventing reoccurrence of one or more symptoms of the disease. In some embodiments, treatment of AD in a subject comprises an administration, e.g., an intravenous infusion, of an anti-amyloid β (Aβ) protofibril antibody. In some embodiments, treatment of AD in a subject comprises a therapeutically effective dose by administration, e.g., an intravenous infusion, of an anti-amyloid β (Aβ) protofibril antibody. As used herein, the term “infusion” refers to an active administration of one or more agents with an infusion time of, for example, approximately 60 minutes. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody, described herein is systemically administered to a human subject via infusion. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody is alternatively administered to the human subject, e.g., by subcutaneous injection. In some embodiments, the subcutaneous injection is a weekly injection. In some embodiments, the subcutaneous injection is a biweekly injection. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody is administered to the human subject by intravenous infusion. In some embodiments, the subject is administered a maintenance dose of a treatment. As used herein, the term “maintenance dose” refers to a dosage administered to a subject to maintain the desired therapeutic effect. In some embodiments, the maintenance dose is administered weekly, every two weeks, monthly, every two months, or every three months (quarterly) or every 24 weeks (every six months or semi-annually). In some embodiments, the maintenance dose comprises an anti-AβAttorney Docket No.08061.0062-00304 protofibril antibody. In some embodiments, the maintenance dose is administered as an intravenous infusion. In some embodiments, the intravenous infusion is a 10 mg / kg dose of BAN2401 administered biweekly. In some embodiments, the intravenous infusion is a 10 mg / kg dose of BAN2401 administered monthly. In some embodiments, the maintenance dose is administered subcutaneously, orally, or nasally. In some embodiments, the maintenance dose is administered subcutaneously. In some embodiments, the maintenance dose is administered as a subcutaneous injection. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a monthly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a quarterly, subcutaneous injection. In some embodiments, the maintenance dose is administered weekly or less frequently, e.g., every two weeks (biweekly), every four weeks, monthly, every six weeks, every eight weeks (2 months), every three months (quarterly) or every six monthly (semi-annually). In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg / 2 mL) of the subcutaneous formulation. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 250 mg. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 250 mg comprising injection of 1.25 mL of 400 mg / 2 mL of a subcutaneous formulation. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 360 mg comprising a single injection of 360 mg of the SC formulation. In some embodiments, the maintenance dose is administered subcutaneously from an autoinjector. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg or 500 mg. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 500 mg comprising two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg / 2 mL) of the subcutaneous formulation. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 500 mg comprising a single injection of 500 mg (e.g., 2.5 mL of 400 mg / 2 mL) of the SC formulation. In some embodiments, the maintenance dose is administered subcutaneously from an autoinjector. In some embodiments, the maintenance dose is administered once or multiple times. In some embodiments, the maintenance dose is administered at a lower dose than during an earlier course of treatment and / or is administered less frequently than during the earlier course of treatment.Attorney Docket No.08061.0062-00304 In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may indicate increasing levels of amyloid in the brain. In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may begin to worsen, e.g. an increasing plasma Aβ42 / 40 ratio, indicating increasing levels of amyloid in the brain. In some embodiments, a subject on a maintenance dose may have a decrease in the Aβ42 / 40 ratio. In some embodiments, a subject is put on a maintenance dose chosen such that the subject may have a decrease in the Aβ42 / 40 ratio but the Aβ42 / 40 ratio may remain above the threshold for amyloid positivity, e.g. for at least one year (e.g., at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 years). In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may begin to increase or a rate of increase may increase. In some embodiments, such a subject may be moved back to a treatment regimen. In some embodiments, a subject may remain on a maintenance dose, e.g., if the increase remains below a tau PET level or rate of increase seen in a control subject who has AD but does not receive an anti-Aβ protofibril antibody. As used herein, the term “prevent” refers to obtaining beneficial or desired results including, but not limited to, prophylactic benefit. For prophylactic benefit, the composition may be administered to a subject at risk of developing Alzheimer’s disease, to a subject having one or more preclinical symptoms but not clinical symptoms of Alzheimer’s disease, or to a subject reporting one or more of the physiological symptoms of Alzheimer’s disease, even though a clinical diagnosis of having Alzheimer’s has not been made. As used herein “prevention” may further include therapeutic benefit, by which is meant eradication or amelioration of the underlying condition being treated or of one or more of the physiological symptoms associated therewith. As used herein, the term “ARIA” refers to amyloid-related imaging abnormality as evaluated using MRI. Without being bound by theory, ARIA may be a consequence of the presence of amyloid in cerebral blood vessel walls, resulting in cerebral amyloid angiopathy (CAA). Without being bound by theory, CAA is present pathologically in most patients with Alzheimer’s, but most patients show no imaging findings (microhemorrhage) or clinical manifestations (intracerebral hemorrhage or inflammatory CAA). Without being bound by theory, removal of amyloid by monoclonal antibodies, e.g., an anti-Aβ protofibril antibody, may increase the risk of ARIA. In some embodiments, ARIA includes amyloid related imaging abnormality edema / effusion (ARIA-E). In some embodiments, ARIA includes amyloid related imaging abnormality hemorrhage (ARIA-H). In some embodiments, the severity of ARIA may be categorized by radiographic imaging, e.g., MRI. In some embodiments, the severity of ARIA may be categorized as mild, moderate, or severe based on radiographic imaging, e.g., MRI. In some embodiments, a mild ARIA-E event comprises FLAIR hyperintensity confined to sulcus and / or cortex / subcortex white matter in one location <5 cm. In some embodiments, a moderate ARIA-E comprises FLAIR hyperintensity 5 to 10 cm in single greatestAttorney Docket No.08061.0062-00304 dimension, or more than 1 site of involvement, each measuring <10 cm. In some embodiments, a severe ARIA-E event comprises FLAIR hyperintensity >10 cm with associated gyral swelling and sulcal effacement, and one or more separate / independent sites of involvement may be noted. In some embodiments, a mild ARIA-H microhemorrhage event comprises ≤ 4 new incident microhemorrhages. In some embodiments, a moderate ARIA-H microhemorrhage event comprises 5 to 9 new incident microhemorrhages. In some embodiments, a severe ARIA-H microhemorrhage event comprises 10 or more new incident microhemorrhages. In some embodiments, a mild ARIA-H superficial siderosis event comprises 1 focal area of superficial siderosis. In some embodiments, a moderate ARIA-H superficial siderosis event comprises 2 focal areas of superficial siderosis. In some embodiments, a severe ARIA-H superficial siderosis event comprises > 2 areas of superficial siderosis. In some embodiments, ARIA-H may include intracerebral hemorrhages > 1 cm. As used herein, the term “clinical decline” refers to a worsening of one or more clinical symptoms of AD. Methods for measuring clinical decline may employ the tests and assays specified herein. In some embodiments, clinical decline is determined by a worsening of ADCOMS. In some embodiments, clinical decline is determined by a worsening of MMSE. In some embodiments, clinical decline is determined by a worsening of ADAS-Cog. In some embodiments, clinical decline is determined by a worsening of FAQ. In some embodiments, clinical decline is determined by a worsening of CDR-SB. In some embodiments, clinical decline is determined by a worsening of Wechsler Memory Scale-IV Logical Memory (subscale) I and / or (subscale) II. In some embodiments, clinical decline is determined by a worsening of CDR score. In some embodiments, clinical decline refers to a worsening in one or more biomarkers of AD or brain measurement (e.g., by PET or MRI), e.g., of brain atrophy and / or amyloid accumulation. As used herein, the term “blood sample” or “blood” refers to a sample of blood, including serum and / or blood plasma from a human subject. In some embodiments, blood will be collected from subjects to evaluate potential biomarkers of AD that may include amyloid fragments and isoforms, tau, and other protein biomarkers (e.g., NFL) for association with AD diagnosis, amyloid or tau load, or disease modification. In some embodiments, subjects are required to fast if possible before collection at Week 96 and Week 216. In other embodiments and / or at other time points, subjects do not require fasting. Pre-AD biomarker levels that may suggest the development of Alzheimer’s disease include, but are not limited to, brain amyloid level, cerebrospinal fluid level of Aβ1-42, cerebrospinal fluid level of total tau, cerebrospinal fluid level of neurogranin, and cerebrospinal fluid level of neurofilament light chain (NfL). 2. Measurement of ARIA The disclosure and methods discussed herein turn in part on the discovery that the risk of an amyloid related imaging abnormality (ARIA) from treatment with anti-Aβ protofibril antibodyAttorney Docket No.08061.0062-00304 such as BAN2401, may depend upon the concomitant use of other medications, such as anticoagulants or thrombolytics, or the presence of brain hemorrhages and status of the brain at baseline. In some embodiments, amyloid related imaging abnormalities (ARIA) can be measured by tools known in the art and may include those described herein. In some embodiments, ARIA is measured by MRI. In some embodiments, ARIA is categorized as ARIA with edema (ARIA-E) or hemosiderin deposition (ARIA-H). In some embodiments, ARIA-E maybe observed on MRI as brain edema or sulcal effusions. In some embodiments, ARIA-H may be observed on MRI as brain microhemorrhages or superficial siderosis. In some embodiments, a patient is monitored for ARIA prior to treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA at least once after treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA more than once after treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA may be monitored at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for ARIA at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, subjects with ARIA experience headache, confusion, and / or seizure and these may be used to identify a subject with ARIA or to indicate further evaluation for ARIA. In some embodiments, ARIA is evaluated at specified intervals during treatment. In some embodiments, ARIA is evaluated when the subject experiences symptoms of ARIA. In some embodiments, maximum serum concentration (Cmax) of anti-Aβ protofibril antibody can be used as a predictor of the risk of ARIA-E. In some embodiments, the use of a subcutaneous formulation may provide a reduced risk of ARIA-E (e.g., due to a lower Cmax) compared to an IV administration. In some embodiments, ARIA may be classified by clinical symptom severity. For example, mild clinical symptom severity may be characterized by discomfort that is noticed, but there is no disruption of normal daily activity. Moderate clinical symptom severity may be characterized by discomfort sufficient to reduce or affect normal daily activity. Severe clinical symptom severity may be incapacitating, leading to an ability to work or to perform normal daily activity. In some embodiments, ARIA may be classified by radiographic severity, e.g., by extent of signal abnormality in MRI. In some embodiments, the radiographic severity depends on signal abnormalities on T2 weighted / fluid attenuation inversion recovery (FLAIR) sequences. In some embodiments, radiographic severity in ARIA-E may be classified as mild if FLAIR hyperintensity isAttorney Docket No.08061.0062-00304 confined to sulcus and / or cortex / subcortex white matter in one location <5 cm. In some embodiments, radiographic severity in ARIA-E may be classified as moderate if FLAIR hyperintensity is 5 to 10 cm in single greatest dimension, or more than 1 site of involvement, each measuring <10 cm. In some embodiments, radiographic severity in ARIA-E may be classified as severe if FLAIR hyperintensity is >10 cm with associated gyral swelling and sulcal effacement. One or more separate / independent sites of involvement may be noted. In some embodiments, ARIA may be classified by radiographic severity, e.g., by the number and / or size of microhemorrhages, and / or by the number and / or size of focal areas of superficial siderosis. In some embodiment, radiographic severity in ARIA-H (microhemorrhage) may be classified as mild if there are ≤ 4 new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (microhemorrhage) may be classified as moderate if there are 5 to 9 new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (microhemorrhage) may be classified as severe if there are 10 or more new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as mild if there is 1 focal area of superficial siderosis. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as moderate if there are 2 focal areas of superficial siderosis. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as severe if > 2 areas of superficial siderosis. In some embodiments, treatment with an anti-Aβ protofibril antibody such as BAN2401 may be continued if the clinical symptom severity and the radiographic severity are mild. For example, for ARIA-E, if the clinical symptom severity is asymptomatic and the radiographic severity is mild, the treatment may be continued. In some embodiments, for ARIA-E, if the clinical symptom severity is mild and the radiographic severity is mild, the treatment may continue based on clinical judgment. In some embodiments, for ARIA-E, if the clinical symptom severity is moderate or severe, the treatment may be suspended. In some embodiments, for ARIA-E, if the radiographic severity is moderate or severe, the treatment may be suspended. In some embodiments, a treatment may be suspended until MRI demonstrates radiographic resolution and symptoms, if present, resolve. A follow-up MRI may be performed to assess for resolution 2-4 months after initial identification of ARIA. In some embodiments, after radiographic stabilization and resolution of symptoms, if any, the treatment may be resumed. In some embodiments, the treatment may be permanently discontinued. In some embodiments, for ARIA-H, if the clinical symptom severity is asymptomatic and the radiographic severity is mild, the treatment may be continued. In some embodiments, for ARIA- H, if the clinical symptom severity is symptomatic, the treatment may be suspended, whether the radiographic severity is mild, moderate, or severe. In some embodiments, a treatment may beAttorney Docket No.08061.0062-00304 suspended until MRI demonstrates radiographic resolution and symptoms, if present, resolve. A follow-up MRI may be performed to assess for resolution 2-4 months after initial identification of ARIA. In some embodiments, after radiographic stabilization and resolution of symptoms, if any, the treatment may be resumed. In some embodiments, the treatment may be permanently discontinued. 3. Measurement of Brain Hemorrhage The disclosure and methods discussed herein turn in part on the discovery that the risk of brain hemorrhage (e.g., microhemorrhage, intracerebral hemorrhage) from treatment with anti-Aβ protofibril antibody such as BAN2401, may depend upon the presence of brain hemorrhages and status of the brain at baseline. In some embodiments, a patient with a brain hemorrhage, e.g., an intracerebral hemorrhage, a microhemorrhage, at baseline is at an increased risk for ARIA. The incidence of brain hemorrhage and the size of a hemorrhage can be measured by tools known in the art and may include those described herein. In some embodiments, brain hemorrhage is measured by MRI. In some embodiments, the brain hemorrhage is measured by number of hemorrhages. In some embodiments, the brain hemorrhage is measured by the size of hemorrhage. In some embodiments, a microhemorrhage is a brain hemorrhage less than 1 cm in diameter as measured on radiographic imaging. In some embodiments, an intracerebral hemorrhage is a brain hemorrhage greater than 1 cm in diameter as measured on radiographic imaging. In some embodiments, a patient is monitored for brain hemorrhage prior to treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline treated with an anti-Aβ protofibril antibody such as BAN2401 is administered a steroid. In some embodiments, a patient is monitored for brain hemorrhage at least once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for brain hemorrhage more than once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, the patient may be monitored after one or more administrations of an anti-Aβ protofibril antibody (e.g., BAN2401), for example, after 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, or more administrations. In some embodiments, the treatment may be continued if the clinical symptom severity and the radiographic severity are asymptomatic or mild. In some embodiments, e.g., if the treatment may be suspended and / or discontinued if the clinical symptom severity and / or the radiographic severity are moderate or severe. In some embodiments, a patient is monitored for brain hemorrhage at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for brain hemorrhage atAttorney Docket No.08061.0062-00304 least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline is not treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient that does not present a microhemorrhage or intracerebral hemorrhage at baseline is treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline treated with an anti-Aβ protofibril antibody, such as BAN2401, is monitored more frequently, e.g., monitored for ARIA, than a patient without a microhemorrhage or intracerebral hemorrhage at baseline. In some embodiments, a patient that presents with CAA at baseline is not treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, treatment is discontinued in a patient who develops CAA. 4. Measurement of Brain White Matter The baseline status of a patient’s white matter in the brain and changes to a subject’s white matter can be measured by tools known in the art and may include those described herein. In some embodiments, the patient’s white matter is assessed by MRI. In some embodiments, the thickness of a patient’s white matter is assessed prior to treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient with a change in white matter from baseline, e.g., a decrease in white matter thickness, has an increased risk of ARIA with treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, a patient’s white matter is monitored for changes at least once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient’s white matter is monitored more than once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, the patient may be monitored after one or more administrations of an anti-Aβ protofibril antibody (e.g., BAN2401), for example, after 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, or more administrations. In some embodiments, the treatment may be continued if the clinical symptom severity and the radiographic severity are asymptomatic or mild. In some embodiments, e.g., if the treatment may be suspended and / or discontinued if the clinical symptom severity and / or the radiographic severity are moderate or severe. In some embodiments, a patient is monitored for changes in white matter at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for changes in white matter at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, a subject that has a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, isAttorney Docket No.08061.0062-00304 not selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who does not have a decrease in brain white matter, e.g., as measured by brain imaging, prior to treatment is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). 5. Selection of patient based on brain hemorrhage and / or brain white matter In some embodiments, a subject’s baseline microhemorrhage or intracerebral hemorrhage status may increase the risk of an ARIA event, intracerebral or microhemorrhage event after administration of an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a patient is selected for treated with an anti-Aβ protofibril antibody such as BAN2401 if that patient has not had or does not currently have an ARIA event and / or intracerebral hemorrhage or microhemorrhage prior to treatment. In some embodiments, a subject who has had or currently has an intracerebral hemorrhage or a microhemorrhage at baseline is not selected for treatment with an anti-Aβ protofibril antibody, (e.g., BAN2401). In some embodiments, a subject exhibiting a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, is not selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who has not exhibited a decrease in brain white matter, e.g., as measured by brain imaging, prior to treatment is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who has had or currently has an intracerebral hemorrhage or a microhemorrhage at baseline is selected for treatment with an anti-Aβ protofibril antibody, (e.g., BAN2401), and is monitored throughout the course of treatment for ARIA events, e.g., more frequently than a subject who has not exhibited a decrease in brain white matter. In some embodiments, a subject exhibiting a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401), and is monitored throughout the course of treatment for ARIA events, e.g., more frequently than a subject who has not exhibited a decrease in brain white matter. In some embodiments, the subject exhibiting a change or decrease in brain white matter may be monitored prior to treatment with an anti-Aβ protofibril antibody (e.g., BAN2401), and prior to one or more infusions with the anti-Aβ protofibril antibody, e.g., prior to the fifth, seventh, and fourteenth infusions. In some embodiments, the subject may be continuously monitored during treatment. 6. Other risk factors for ARIA In some embodiments, other factors may affect a subject’s risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. A subject may be monitored for risk factors prior to or during administration of the anti-Aβ protofibril antibody. InAttorney Docket No.08061.0062-00304 some embodiments, a subject who is found to have a risk factor prior to treatment may be excluded or treated with an alternate therapy from an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject having a risk factor may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA, e.g., monitored more frequently, during the treatment than a subject who does not have the risk factor. In some embodiments, ARIA may be monitored by radiographic imaging of the subject’s brain (e.g., by MRI). In some embodiments, the treatment may be discontinued if a subject is found to develop ARIA. In some embodiments, a subject who is not found to have a risk factor prior to treatment may be selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, subjects who are carriers for the ApoE4 allele may have an increased risk of ARIA during treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. Accordingly, in some embodiments, the subject’s ApoE4 status is assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401) by a DNA test of a body sample such as blood or a buccal swab. In some embodiments, a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who is not a carrier for the ApoE4 allele. In some embodiments, treatment may be discontinued if a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) is found to develop ARIA. In some embodiments, a subject who is not a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with a higher blood pressure, also called higher mean arterial pressure (e.g., prior to and / or during treatment), as compared to a control (e.g., a blood pressure in a healthy subject or a threshold blood pressure measurement based on a population average), may have increased risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s mean arterial blood pressure is assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by auscultation, by measuring oscillations in blood flow and calculating blood flow, or measuring blood pressure with an invasive probe inserted directly into the lumen of an artery. In some embodiments, a subject who has a higher mean arterial pressure as compared to a control (e.g., a healthy subject) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a high mean arterial pressure may be 130-139 mmHg / 80-89 mmHg or higher. In some embodiments, a high mean arterial pressure may be 140 mmHg / 90 mmHg or higher. In someAttorney Docket No.08061.0062-00304 embodiments, a high mean arterial pressure may be 180 mmHg / 120 mmHg or higher. In some embodiments, a subject who has a higher mean arterial pressure as compared to a control may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have a higher mean arterial pressure as compared to a control. In some embodiments, the treatment may be discontinued if a subject’s blood pressure increases during treatment and / or the subject with higher mean arterial pressure is found to develop ARIA. In some embodiments, a subject who does not have higher mean arterial pressure is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with a greater amyloid burden (e.g., as determined by amyloid PET, or by a fluid biomarker such as an Aβ 42 / 40 ratio, e.g., measured prior to and / or during treatment), as compared to a control (e.g., a healthy subject), may have increased risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s amyloid burden is assessed prior to treatment (e.g., treatment with an anti- Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by PET imaging for amyloid PET, or by detection of a a fluid biomarker such as an Aβ 42 / 40 ratio. In some embodiments, a subject who has a higher amyloid burden as compared to a control (e.g., a healthy subject) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who has a higher amyloid burden as compared to a control may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have a higher amyloid burden as compared to a control. In some embodiments, the treatment may be discontinued if a subject develops a higher amyloid burden and / or the subject with a higher amyloid burden is found to develop ARIA. In some embodiments, a subject who does not have higher amyloid burden is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with cortical superficial siderosis (e.g., prior to and / or during treatment) may have increased risk of ARIA-E when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s brain is scanned for superficial siderosis assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by imaging (e.g., by MRI). In some embodiments, a subject who has cortical superficial siderosis may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who has cortical superficial siderosis may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have cortical superficial siderosis. In some embodiments, the treatment may be discontinued if a subject develops cortical superficial siderosis and / or the subject with cortical superficial siderosis is found to develop ARIA-E. In some embodiments, a subject who does not have cortical superficial siderosis is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401).Attorney Docket No.08061.0062-00304 7. Steroid use in treating severe ARIA In some embodiments, a patient with an increased risk of an intracerebral hemorrhage or microhemorrhage event and / or ARIA is administered a steroid before and / or during treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient exhibiting severe ARIA during treatment with an anti-Aβ protofibril antibody (e.g., BAN2401) is administered a steroid. Steroid treatment may be by any known route, e.g., intravenous and / or oral. Steroid dose and regimen may be according to those known in the art. In some embodiments, a patient with a severe radiographic or symptomatic ARIA-E is administered a steroid at a dose and / or frequency consistent with the standard of care known by one of ordinary skill in the art. 8. Use with anticoagulants, antiplatelet agents, and thrombolytic agents Without being bound by theory, it has been surprisingly found that patients concurrently administered certain anticoagulant or thrombolytic agents may have an equal or reduced risk of an ARIA event, cerebral hemorrhage, or microhemorrhage to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. Again, without being bound by theory, some patients on certain anticoagulant or thrombolytic agents may have improved therapeutic outcomes when administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, an AD subject or early AD subject is administered or treated with an anticoagulant or thrombolytic (e.g., aspirin, antiplatelet, anticoagulant, fibrinolytic, tissue plasminogen activator) medication. As used herein, a thrombolytic and an antithrombotic are used interchangeably. In some embodiments, the thrombolytic agent is aspirin. In some embodiments, the thrombolytic agent is an antiplatelet. In some embodiments, the thrombolytic agent is an anticoagulant. In some embodiments, the thrombolytic agent is a fibrinolytic agent. In some embodiments, the thrombolytic agent is a tissue plasminogen activator. In some embodiments, a subject treated with an anticoagulant medication is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with an anticoagulant medication and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebral hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject treated with an antiplatelet medication is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with an antiplatelet medication and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebral hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject treated with aspirin is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with aspirin and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebralAttorney Docket No.08061.0062-00304 hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject receiving the anti-Aβ protofibril antibody such as BAN2401 is not administered an anticoagulant or a thrombolytic agent. In some embodiments, a subject treated with an anticoagulant or a thrombolytic agent is not selected for treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 is not administered a tissue plasminogen activator. In some embodiments, a subject treated with a tissue plasminogen activator is not selected for treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments a patient treated with a tissue plasminogen activator is administered an anti-Aβ protofibril antibody such as BAN2401, e.g., with additional monitoring for ARIA. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 that is also receiving an anticoagulant or a thrombolytic agent is monitored for an ARIA event. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 that is also receiving an anticoagulant or a thrombolytic agent will stop receiving the anti-Aβ protofibril antibody until treatment with the anticoagulant or thrombolytic agent is discontinued. In some embodiments, a subject’s brain may be monitored (e.g., by MRI) at any time during treatment with the anti-Aβ protofibril antibody such as BAN2401. Extra monitoring may be performed, for example, when the subject has factors that indicate an increased risk for intracerebral hemorrhage, such as subjects who are on anticoagulant therapy. In some embodiments, a subject who is administered a steroid may be monitored further, e.g., by MRI. 9. Selection of patient and monitoring for change in regimen based on biomarkers a. Measurement of Tau PET The disclosure and methods discussed herein turn in part on the discovery that biomarker, such as a tau PET level, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody, alone or in combination of other biomarkers. A treatment comprising an anti-Aβ protofibril antibody such as BAN2401 can lead to a reduced rate of tau accumulation, as measured by a tau PET level (e.g., as measured by tau PET imaging), e.g., in a brain region such as a temporal region, as compared to a control patient. In some embodiments, this correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Without being bound by theory, a tau PET level (e.g., a tau PET standard uptake value ratio (SUVr)) may be used, in various embodiments, as a less invasive and / or additional biomarker forAttorney Docket No.08061.0062-00304 refining the measurement of treatment efficacy and / or to allow for monitoring and treatment decisions. Such decision may include whether to increase or decrease the amount of an anti-Aβ protofibril antibody being administered, whether to increase or decrease the frequency of administration, whether to introduce a further therapeutic agent, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody. As used herein, the term “tau PET” refers to tau positron emission tomography imaging. In some embodiments, tau PET imaging (also referred to as a PET scan) is performed to assess for tau pathology. In some embodiments, tau PET is assessed with a PET tracer and uses the same tracer in follow-up assessments. In some embodiments, the PET imaging uses a [18F]MK-6240tracer. Tau positron emission tomography (PET) imaging can be used to confirm the presence of tau pathology in the brain of early AD subjects in the screening phase of the study and / or to evaluate the effects of the at least one anti-Aβ protofibril antibody on amyloid levels in the brain, both by whole brain analysis (e.g., the average of 5-6 cortical regions) and brain region analysis (e.g., in a temporal brain region). In some embodiments, the PET scan uses a [18F]MK-6240 (florquinitau) tracer. In some embodiments, tau load can be identified by a PET imaging uptake visual read, e.g., by a trained radiologist. In embodiments, regions of the brain are assessed for uptake of the imaging agent. In some embodiments, the temporal region is assessed for a tau PET level. In some embodiments, the frontal region is assessed for a tau PET level. In some embodiments, the parietal region is assessed for a tau PET level. In some embodiments, the occipital region is assessed for a tau PET level. In some embodiments, the cingulate region is assessed for a tau PET level. In some embodiments, the temporal region comprises the medial temporal region. In some embodiments, the medial temporal region comprises the hippocampus, the entorhinal cortex, the parahippocampus, and / or the anterior medial / lateral temporal lobes. In some embodiments, the temporal region comprises the meta-temporal region. In some embodiments, the meta-temporal region comprises the amygdala, the entorhinal cortex, the parahippocampus, the middle / interior and posterior temporal lobe, and / or the fusiform region. In some embodiments, the temporal region comprises the temporal lobe. In some embodiments, the temporal lobe comprises the superior anterior / posterior temporal lobe, the middle / inferior temporal lobe, the posterior temporal lobe, and / or the fusiform cortex. In some embodiments, the whole cortical gray matter is assessed for a tau PET level. In some embodiments, the reference region used for assessing a tau PET level is the ventral cerebellum (Cb). In some embodiments, a “tau PET level” can be identified by a standard uptake value ratio (SUVr) as compared to a reference region as measured by tau PET imaging. As used herein, a “tau PET level”, “tau level in a brain” and “tau load” are used interchangeably. As used herein a tau PET level refers to a measurement of a level of tau in a brain region, e.g., a temporal region, by PET. Methods for calculating tau PET SUVr are known in the art and may include those described herein.Attorney Docket No.08061.0062-00304 In some embodiments, a Standard Uptake Value Ratio Quantitative analysis of amyloid levels is completed using PMOD PNEURO Biomedical Image Quantification Software (PMOD Technologies, Zurich, Switzerland). In some embodiments, PET images are first assessed for subject movement in the X, Y, and Z planes and corrected for motion, if needed, before individual images (e.g., 5-minute emission frames) are averaged, e.g., using a PMOD Averaging Function (PET frames averaged to increase the signal to noise ratio). In some embodiments, corresponding MRIs from subjects are prepared (e.g., using matrix size reduction processing, cropping of the MRI to include only the brain, segmentation to separate images into binary maps of gray matter, white matter, and CSF, and stripping the image of skull leaving only brain mask). In some embodiments, the averaged PET images and prepared MRIs are matched using the PMOD Matching Function, placing the images in the same orientation. In some embodiments, a Brain Normalization function, e.g., as provided by PMOD software, is used along with Brain Norm and Rigid Matching transformation matrices, to produce an averaged PET. In some embodiments, this averaged PET which is normalized to the MNInst space (Senjem et al, 2005) that is in the same orientation as the subject’s segmented MRI for quantitative analysis. In some embodiments, the PMOD Mask Function is used to mask the brain and zero the image outside of the mask to create a Normalized Gray Matter PET and a Normalized White Matter PET. Standard uptake values (SUVs) may be calculated for all gray matter mapped regions and the 3 white matter regions (pons, cerebellar white, and subcortical white) using PMOD software calculated using the normalized PET, subject weight, and injected dose of tracer to arrive at the units of SUVs. In some embodiments, the SUVr is the ratio of the global cortical average as compared to a reference region of choice. In some embodiments, a whole cerebellum mask is used as the reference region. In some embodiments, the reference region is subcortical white matter, ventral cerebellum, derived whole cerebellum, whole cerebellum adjusted by subcortical white matter, cerebellar gray matter, and composite reference regions consisting of cerebellar cortex, pons subcortical white matter, and cerebella white matter. In some embodiments, the adjusted mean change from baseline is measured prior to treatment and at least once after the start of treatment, e.g., over a period of at least 6 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 12 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 13 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 18 months after an initial dose of a treatment. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.10. In some embodiments, after administration of the firstAttorney Docket No.08061.0062-00304 dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.05. In some embodiments, 13 months after an initial dose of a treatment, the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.05. In some embodiments, 18 months after an initial dose of a treatment, the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. Additional methods for measuring tau by positron emission tomography (PET) are known in the art. Methods may include the TauIQalgorithm (see, e.g., Whittington et al., J. Nucl Med.2021 Sep 1;62(9):1292-1300 for quantitatively measuring tau PET radiotracers). The measurement of a tau PET level may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as one or more measurement in a biofluid (e.g., p-tau181 and / or a ratio of Aβ1-42 to Aβ1-40), PET measurement of Aβ (e.g., via radiotracer uptake), MRI evaluation of Aβ plaque, and / or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring a tau PET level and determining a subject is suitable for treatment because of a higher tau PET level than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject).In some embodiments, a subject is selected for treatment because of a high tau PET level in a region of the brain of the subject, wherein the tau PET level is greater than a subject who does not have AD. In some embodiments, a subject is selected for treatment because of a high tau PET level in the temporal region of the brain of the subject, wherein the tau PET level is greater than 1.4 as measured by amyloid PET SUVr. In some embodiments, a subject is selected for treatment because of a high tau PET level in the temporal region of the brain of the subject, wherein the tau PET level is greater than 1.5 as measured by amyloid PET SUVr. In some embodiments, the measurement of a tau PET level may be used in place of another method of measuring brain tau levels and / or in place of another marker of Aβ. In some embodiments, the measurement of a tau PET level may be used in conjunction with measuring one or more additional markers. In some embodiments, a patient may be monitored by one or more additional biomarkers such as, but not limited to: (a) tau detected by PET scan from either a visual read or semiquantitative thresholds (SUVr or centiloid); (b) cerebrospinal fluid (CSF) total tau (t-tau); and / or (c) blood biomarkers (such as plasma total tau (T- tau), and / or phosphorylated tau (P-tau)(e.g., p-tau181)). In some embodiments, a patient’s tau PET level may be monitored in conjunction with one or more of a ratio of Aβ1-42 to Aβ1-40 and / or a p- tau181 measurements in a fluid sample, e.g., a blood sample. In some embodiments, the combination comprises a serum or plasma GFAP measurement. In some embodiments, the measurement of a tau PET level may be used in place of another method of measuring brain tau levels for determiningAttorney Docket No.08061.0062-00304 treatment efficacy and / or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, a tau PET level may be used to calculate a relative change from a baseline measurement (e.g., a measurement of a tau PET level before beginning a treatment). In some embodiments, a tau PET level measurement may be repeated after the start of a treatment regimen to monitor treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over a 13-month period in a region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over an 18-month period in a region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over a 13-month period in the temporal region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over an 18-month period in the temporal region of the brain indicates treatment efficacy. In some embodiments, a rate of change of a tau PET level is calculated based on two measurements from a subject. In some embodiments, a rate of change of a tau PET level is calculated based on more than two measurements from a subject. In some embodiments, a rate of change of a tau PET level indicates the rate of tau accumulation in the brain of a subject. In some embodiments, a rate of change of a tau PET level is calculated based on at least two measurements from a subject, wherein one measurement is taken from a subject before a treatment, and a second measurement is taken after the start of treatment, wherein treatment continues for at least 13 or 18 months after an initial dose of a treatment. In some embodiments, the rate of change of the tau PET level is compared to the rate of change of the tau PET level in an untreated control subject who has AD and has not received treatment. In some embodiments, a lower rate of tau PET increase relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 6-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 12-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 13-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over an 18-month period relative to an untreated control subject indicates treatment efficacy. Methods of measuring clinical efficacy or monitoring a treatment may employ a set threshold to determine a change in brain tau levels, e.g., to identify a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the tau PET level threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as an amyloid PET scan, a CSF or serum or plasmaAttorney Docket No.08061.0062-00304 biomarker, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, a tau PET level may be used in place of another method of measuring brain tau levels. In some embodiments, a tau PET level greater than a threshold level is used to determine if a patient is suitable for treatment. In some embodiments, a tau PET level threshold is about 1.4. In some embodiments, a tau PET level threshold is about 1.5. In some embodiments, a subject is selected for treatment with an anti-amyloid β (Aβ) protofibril antibody, wherein the subject has a tau PET level in a region of the brain greater than about 1.4. In some embodiments, a subject is selected for treatment with an anti-amyloid β (Aβ) protofibril antibody, wherein the subject has a tau PET level in a region of the brain greater than about 1.5. In some embodiments, the region of the brain is the temporal region. In some embodiments, the region of the brain is the temporal lobe. In some embodiments, the region of the brain is the meta-temporal lobe. In some embodiments, the region of the brain is the medial-temporal lobe. b. Measurement of Aβ42 / 40 ratio The disclosure and methods discussed herein depend in part on the discovery that a biomarker, such as an Aβ42 / 40 ratio, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody, alone or in combination of other biomarkers. Aβ42 and 40 be measured to calculate a ratio in blood samples, as disclosed in PCT / US2022 / 073576, which herein is incorporated by reference. A treatment comprising an anti-Aβ protofibril antibody such as BAN2401 can lead to an increase in the Aβ42 / 40 ratio that correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Methods for measuring the Aβ42 / 40 ratio are known in the art, such as assays using LC MS / MS. Methods may include the PrecivityADTMassay (see, e.g., Kirmess et al., J. Clinica Chimica Acta 519: 267-275 (2021)) and the Sysmex assay (https: / / www.eisai.com / news / 2019 / news201990.html) for measuring Aβ42 and Aβ40 in a sample to use in calculating a ratio. The measurement of the Aβ42 / 40 ratio may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as a tau PET level, a PET measurement of Aβ radiotracer update, MRI evaluation of Aβ plaque, and / or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring an Aβ42 / 40 ratio and determining a subject is suitable for treatment because of a lower ratio than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject). In some embodiments, the measurement of an Aβ42 / 40 ratioAttorney Docket No.08061.0062-00304 may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining a subject is suitable for treatment. In some embodiments, the measurement of an Aβ42 / 40 ratio may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining treatment efficacy and / or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, an Aβ42 / 40 ratio measurement may employ a relative change from baseline measurement. In some embodiments, an Aβ42 / 40 ratio measurement may employ a set threshold to determine a change in brain amyloid levels, e.g., to identify a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as a PET scan, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, an Aβ42 / 40 ratio threshold may be used in place of another method of measuring brain amyloid levels, such as a PET scan, to determine amyloid positivity. In some embodiments, an Aβ42 / 40 ratio threshold is at or about 0.09, 0.091, 0.092, 0.093, 0.094, 0.095, 0.096, 0.097, 0.099, 0.1. In some embodiments, the threshold is about 0.092. In some embodiments, the threshold is 0.092. In some embodiments, the threshold is about 0.094. In some embodiments, a decrease in the Aβ42 / 40 ratio below a threshold value may indicate a need to continue treatment or to select an increase in a dosing regimen. In some embodiments, an increase in the Aβ42 / 40 ratio above a threshold value may be used to indicate a treatment may be terminated (e.g., terminated in favor of a maintenance regimen) and / or to otherwise to determine a decrease in a dosing regimen or discontinuation in treatment. In some embodiments, a decrease in the Aβ42 / 40 ratio below a threshold value may be used to determine whether to discontinue a maintenance dosing regimen, e.g., and return to the prior treatment regimen. c. Measurement of a p-tau level The disclosure and methods discussed herein depend in part on the discovery that a biomarker, such as a p-tau level, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody, but also in combination of other biomarkers, such as a phosphorylated tau (p-tau) level, including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and / or 231 (P-tau231), and / or the ratio of P-tau181 / NP-tau181, and / or the ratio of P-tau217 / NP-tau217). A p-tau level can be measured in CSF, serum, or plasma, as disclosed in PCT / US2022 / 079571, which herein is incorporated by reference. A treatment comprising an anti-Attorney Docket No.08061.0062-00304 Aβ protofibril antibody such as BAN2401 can lead to a decrease in a p-tau181 level that correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Methods for measuring p-tau ratio are known in the art, such as immunoassay (e.g., a Quanterix™ Simoa®p-tau assay) and / or mass spectrophotometry (IP / LC-MS / MS) based technology methods. Plasma p-tau181 is elevated in early stages of AD as determined by Braak staging (I-II) and continues to increase as the disease progresses into Braak stage V-VI (Janelidze et al., “Plasma P- tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia,” Nat. Med., 26(3):379-386 (2020)). The biomarker highly correlates with amyloid PET and Tau PET and has demonstrated a 3.5-fold elevation in AD compared to control, with an intermediate increase in the MCI group, and appears to differentiate patients with clinically diagnosed AD from other tauopathies as well (Thijssen et al., “Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration,” Nat. Med., 26(3):387-397 (2020); Janelidze et al.). The measurement of the p-tau level (e.g., a p-tau181 level, a p-tau217 level, and / or a p- tau231 level, and / or the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217) may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as a tau PET level, a PET measurement of Aβ radiotracer update, MRI evaluation of Aβ plaque, and / or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring the level of p-tau (e.g., a p-tau181 level, a p-tau217 level, and / or a p-tau231 level, and / or the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np- tau217) and determining a subject is suitable for treatment because of a higher level than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject). In some embodiments, the measurement of the level of p-tau (e.g., a p- tau181 level, a p-tau217 level, and / or a p-tau231 level, and / or the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217) may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining a subject is suitable for treatment. In some embodiments, the measurement of the level of p-tau (e.g., a p-tau181 level, a p-tau217 level, and / or a p-tau231 level, and / or the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217) may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining treatment efficacy and / or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, a plasma or serum p-tau181 level measurement may employ a relative change from baseline measurement. In some embodiments, a change in the p-tau181 level may be used to evaluate treatment efficacy. In some embodiments, a decrease in the level of p-tau181 indicates treatment efficacy, e.g., a reduction in brain amyloid levels. In some embodiments, a p-Attorney Docket No.08061.0062-00304 tau181 level measurement may employ a set threshold to determine a change in brain amyloid levels, e.g., to identify and / or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as a PET scan, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, a p-tau181 level threshold may be used in place of another method of measuring brain amyloid levels, such as a PET scan. In some embodiments, a p-tau181 level threshold at or above about 2.2 to 2.3 pg / mL is used to identify and / or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In some embodiments, a p-tau181 level threshold at or above about 2.2 pg / mL is used to identify and / or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In some embodiments, a p-tau181 level threshold at or above about 2.3 pg / mL is used to identify and / or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In certain such embodiments, the p-tau181 level is measured using a Quanterix™ Simoa®p-tau assay. In some embodiments, the threshold is about 2.3 pg / mL. In some embodiments, the threshold is about 2.2 pg / mL. In some embodiments, an increase in the p-tau181 level above a threshold value may indicate a need to continue treatment or to select an increase in a dosing regimen. In some embodiments, a decrease in the p-tau181 level below a threshold value may be used to indicate a treatment may be terminated (e.g., terminated in favor of a maintenance regimen) and / or to otherwise to determine a decrease in a dosing regimen or discontinuation in treatment. In some embodiments, p-tau 181 levels may be measured in the blood, e.g., where a blood- based test is faster, easier, and / or more cost effective than an assay of cerebrospinal fluid (CSF) or imaging methods. p-tau 181, in particular, has been shown to correlate with brain amyloid burden, tau accumulation, and clinical progression in pre-clinical and early AD individuals (Wang YL et al., Plasma p-tau181 Level Predicts Neurodegeneration and Progression to Alzheimer's Dementia: A Longitudinal Study. Front Neurol.4382021;12:695696.; Jack CR et al., Predicting amyloid PET and tau PET stages with plasma biomarkers. Brain.2023;146:2029-44). In some embodiments, a higher tau PET level (e.g., p-tau 181) in a subject as compared with a healthy control subject indicate that a subject with pre-AD or at risk for AD or with early AD will progress over the next 18 months and / or may predict 36-month progression from Aβ+ mild cognitive impairment to AD. d. Plasma or serum level of GFAP In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in glial fibrillary acidic protein (GFAP) in the plasma or serum of a subject. Without being bound by theory, the GFAP level may be used as a marker of astrocyte activation. The GFAP levelAttorney Docket No.08061.0062-00304 may be measured by techniques known in the art, such as an immunoassay (e.g., a Quanterix™ Simoa® assay) and / or mass spectrophotometry (IP / LC-MS / MS) based technology methods. In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in plasma or serum levels of GFAP in the subject. In some embodiments, the administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, in the plasma or serum level of GFAP. In some embodiments, a serum level of GFAP, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, additional biomarkers in combination with a decreasing GFAP level over the same period, may indicate an effective treatment. In some embodiments, improvements in other biomarkers in combination with a decreasing GFAP level over the same period, may indicate an effective treatment. In some embodiments, improvements in other biomarkers in combination with a decreased GFAP level relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. e. Cerebrospinal Fluid Level of Neurogranin In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in cerebrospinal fluid level of neurogranin in the subject. In some embodiments, the administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, in cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of neurogranin after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising aAttorney Docket No.08061.0062-00304 therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, cerebrospinal fluid level of neurogranin after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 25 pg / mL, at least about 30 pg / mL, at least about 35 pg / mL, at least about 40 pg / mL, at least about 45 pg / mL, at least about 50 pg / mL, at least about 55 pg / mL, at least about 60 pg / mL, or at least about 65 pg / mL, relative to baseline, cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg / mL, relative to baseline, cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 25 pg / mL, at least about 30 pg / mL, at least about 35 pg / mL, at least about 40 pg / mL, at least about 45 pg / mL, at least about 50 pg / mL, at least about 55 pg / mL, at least about 60 pg / mL, or at least about 65 pg / mL, relative to baseline, of cerebrospinal fluid level of neurogranin after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administering to a subject a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 65 pg / mL, relative to baseline, of cerebrospinal fluid level of neurogranin after 18 months of administration of the composition. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody is 10 mg / kg. In some embodiments, the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi- weekly or monthly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered monthly. In some embodiments, a cerebrospinal fluid level of neurogranin, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, inAttorney Docket No.08061.0062-00304 combination with a decreasing cerebrospinal fluid level of neurogranin over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of neurogranin over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreased cerebrospinal fluid level of neurogranin relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. f. Level of Neurofilament Light Chain In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, in cerebrospinal fluid level and / or the plasma or serum level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, or at least 50%, relative to placebo, in cerebrospinal fluid level and / or the plasma or serum level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, in cerebrospinal fluid level and / or the plasma or serum level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, of at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, or at least 50%, relative to baseline, in cerebrospinal fluid level and / or the plasma or serum level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of more than about 35 pg / mL, about 40 pg / mL, about 45 pg / mL, about 50 pg / mL, about 55 pg / mL, about 60 pg / mL, about 65 pg / mL, about 70 pg / mL, about 75 pg / mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of no more than about 75 pg / mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain.Attorney Docket No.08061.0062-00304 In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of more than about 35 pg / mL, about 40 pg / mL, about 45 pg / mL, about 50 pg / mL, about 55 pg / mL, about 60 pg / mL, about 65 pg / mL, about 70 pg / mL, about 75 pg / mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of no more than about 75 pg / mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is 10 mg / kg. In some embodiments, a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi-weekly or monthly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered monthly. In some embodiments, an additional biomarker and a plasma or serum level of neurofilament light, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing plasma or serum level of neurofilament light over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing plasma or serum level of neurofilament light over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, t in combination with a decreased plasma or serum level of neurofilament light relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. g. Cerebrospinal Fluid Level of Phospho-Tau In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of phospho-Tau (p-tau). In some embodiments, administrationAttorney Docket No.08061.0062-00304 to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, at least 10%, at least 11%, at least 12%, or at least 13% relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, at least 10%, at least 11%, at least 12%, or at least 13%, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg / mL, at least about 70 pg / mL, at least about 75 pg / mL, at least about 80 pg / mL, at least about 85 pg / mL, at least about 90 pg / mL, or at least about 95 pg / mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 95 pg / mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg / mL, at least about 70 pg / mL, at least about 75 pg / mL, at least about 80 pg / mL, at least about 85 pg / mL, at least about 90 pg / mL, or at least about 95 pg / mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 95 pg / mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody is 10 mg / kg. In some embodiments, the composition comprising a therapeuticallyAttorney Docket No.08061.0062-00304 effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi- weekly or monthly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg / kg of BAN2401 is administered monthly. In some embodiments, an additional biomarker and cerebrospinal fluid level of phospho- Tau, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and / or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of phospho-Tau over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of phospho-Tau over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreased cerebrospinal fluid level of phospho-Tau relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. h. Brain Volume In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in an improvement, relative to placebo, of total hippocampal atrophy as measured by volumetric MRI (vMRI). In some embodiments, a subject’s brain volume (e.g., total ventricular volume, left and / or right ventricular volume, total volume, right and / or left hippocampal volumes, cortical thickness) is measured before treatment. In some embodiments, a subject’s brain volume (e.g., total ventricular volume, left and / or right ventricular volume, total volume, right and / or left hippocampal volumes, cortical thickness) is measured at 6,12, and / or 18 months after treatment. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in an improvement, relative to placebo, of brain volume atrophy as measured by vMRI. 10. Subjects having AD, suspected of having AD, or at risk of developing AD Subjects treated herein include those having AD or suspected of having AD. In some embodiments, the subject shows changes (e.g., an increase, a decrease, a change in the rate and / or extent of an increase, or a change in the rate and / or extent of the decrease) in one or more biomarkers associated with AD pathology (e.g., the biomarkers described above), as compared with a referenceAttorney Docket No.08061.0062-00304 measurement. In some embodiments, the reference measurement may be a measurement taken from the same subject, e.g., at an earlier point in time, or a measurement in a part of the subject’s body, tissue, or fluids where the biomarkers levels do not change in response to AD pathology. In some embodiments, the reference measurement may be a measurement taken from another subject, such as a healthy control subject, or may be an average of measurements taken from more than one reference subject. In some embodiments, the subject may show a change and / or a difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment, e.g., one or more of (a) increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), (b) increased tau in the brain, e.g., as measured by positron emission tomography (PET), (c) decreased cerebrospinal fluid levels of Aβ1- 42 (e.g., a decreased ratio of Aβ1-42 / 1-40) and / or increased total tau, phosphorylated tau isoforms (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p-tau181 / np-tau181, and / or the ratio of p- tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and (d) decreased blood serum or plasma levels of Aβ1-42 (e.g., a decreased ratio of Aβ1-42 / 1-40 in the plasma or serum), and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P- tau231), ratio of P-tau181 / NP-tau181, and / or ratio of P-tau217 / NP-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL), as compared to a reference measurement (e.g., measurement from a healthy control). In some embodiments, the subject may show a change in the ratio of phosphorylated to non-phosphorylated Tau 217 (P-Tau217 / NP-Tau217 ratio, also called P-Tau217R or pTau217R) in blood plasma or serum, e.g., the ratio may be increased in subjects who have, are suspected of having, or are at risk of developing AD. Without being bound by theory, biomarkers as disclosed herein may be effective for predicting amyloid PET status (Rissman et al., 2024, Alzheimers & Dementia, 20(2): 1214-1224; Janelidze et al., 2022, Alzhimer’s & Dementia, 18:283-293) and for detecting and diagnosing AD (Hampel et al., 2023, Neuron, 111(18):2781-2799). In some embodiments, at least one of p-tau217 / np-tau217, Aβ42 / Aβ40, and p-tau181 / np-tau181 may be used to predict amyloid PET status. In some embodiments, a measurement of p-tau217 and / or Aβ42 / Aβ40 may be used to predict amyloid PET status. In some embodiments, a combination of p- tau217 and Aβ42 / Aβ40 may be used to predict amyloid PET status. In some embodiments, the ratios of p-tau217 / np-tau217 and Aβ42 / Aβ40 may be used in combination to predict amyloid PET status. In some embodiments, the subject is amyloid-positive, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, and / or retinal amyloid accumulation. In some embodiments, a subject has AD, e.g., has been diagnosed with AD. For example, the subject may have been diagnosed with (a) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia; (b)Attorney Docket No.08061.0062-00304 mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; (c) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; (d) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; (e) mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or (f) mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject has early AD. The subject with early AD may have symptoms ranging in severity from mild cognitive impairment due to AD – intermediate likelihood to mild Alzheimer’s disease dementia. In some embodiments, subjects with early AD have MMSE scores of 22 to 30 and Clinical Dementia Rating (CDR) global range 0.5 to 1.0. In some embodiments, a subject is suspected of having AD, e.g., based on one or more biomarkers and / or cognitive symptoms of dementia. In some embodiments, a subject is at risk for developing AD but has not yet exhibited cognitive symptoms of dementia. For example, a subject may have risk factors related to age or genetic mutations. In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is at least 65 years old, e.g., 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing. In some embodiments, a subject at risk for AD has elevated brain amyloid, e.g., as measured by and / or confirmed by PET assessment, but does not exhibit any detectable cognitive symptoms. In some embodiments, a subject at risk for AD has a change in a biomarker such as amyloid PET; tau in the brain, e.g., as measured by positron emission tomography (PET), cerebrospinal fluid levels of one or more of Aβ1-42 (or a ratio of Aβ1-42 / 1-40 in the cerebrospinal fluid), total tau, phosphorylated tau (P-tau) isoforms (e.g., P- tau181, P-tau217, and / or P-tau231), the ratio of P-tau181 / NP-tau181, the ratio of P-tau217 / NP- tau217, neurogranin, and neurofilament light chain (NfL), and / or a change in a blood serum or plasma levels of one or more of Aβ1-42 (or a ratio of Aβ1-42 / 1-40), total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), the ratio of P-tau181 / NP-tau181, and / or the ratio of P-tau217 / NP-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL), relative to a control subject or population. In some embodiments, a subject at risk for developing AD may have pre-AD (also referred to as preclinical AD, in which subjects are cognitively unimpaired but have elevated amyloid in theAttorney Docket No.08061.0062-00304 brain, e.g., as based on a change in one or more biomarkers associated with AD pathology). For example, the subject may show a change in one or more biomarkers associated with AD pathology, but no cognitive impairment, e.g., as measured by clinical symptoms of AD. In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments. In some embodiments, the subject has a Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII) score better than one standard deviation below age-adjusted mean in the WMS-IV LMII; namely a score of greater than 15 for a subject of age ranging from 50 to 64 years, of greater than 12 for a subject of age ranging from 65 to 69 years, of greater than 11 for a subject of age ranging from 70 to 74 years, of greater than 9 for a subject of age ranging from 75 to 79 years, and of greater than 7 for a subject of age ranging from 80 to 90 years. 11. Anti-Aβ protofibril antibodies In some embodiments, an antibody binding to Aβ (also called an anti-Aβ antibody) is an antibody that binds to any form (e.g., conformation) of Aβ, such as Aβ monomers, oligomers (e.g., different forms of Aβ oligomers such as dimers, trimers, tetramers, pentamers, hexamers, nonamers, dodecamers), a paranucleus (e.g., a partially-folded monomer that forms a nucleus for fibril elongation), protofibrils, or mature fibrils. In some embodiments, an anti-Aβ antibody may bind to more than one form of Aβ. For example, an exemplary anti-Aβ antibody may be a pan-Aβ antibody, such as a pan-AβpE3 antibody that reacts with high molecular weight oligomers, protofibrils, and fibrillar forms of Aβ that are found in different plaque types. In some embodiments, an anti-Aβ antibody may bind preferentially to a specific form of Aβ. For example, an exemplary Aβ antibody may be an anti-Aβ protofibril antibody that binds to at least to protofibrils. In some embodiments, an anti-Aβ protofibril antibody may bind preferentially to protofibrils and may also bind to other forms of Aβ. In some embodiments, an anti-Aβ protofibril antibody may preferentially bind to protofibrils as compared to other forms of Aβ. In some embodiments, an anti-Aβ protofibril antibody may preferentially bind to protofibrils, and not to other forms of Aβ. In some embodiments, any anti-Aβ protofibril antibody may be used in the methods disclosed herein. In some embodiments, the antibody comprises one or more of the sequences listed in Tables 1-4, e.g., comprising a complete set of 6 complementarity determining regions (CDRs) and / or a complete set of variable regions and / or a complete set of heavy and light chain sequences from the tables. In some embodiments, the anti-Aβ protofibril antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regions (LCDR1 , LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6Attorney Docket No.08061.0062-00304 (LCDR3). In some embodiments, the anti-Aβ protofibril antibody comprises a heavy chain variable region comprising an amino acid sequence of SEQ ID NO: 7 and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 8. In some embodiments, the anti-Aβ protofibril antibody comprises human heavy and light chain variable region frameworks. In some embodiments, the anti-Aβ protofibril antibody comprises a human IgG1 heavy chain constant region, and a human Ig kappa light chain constant region. In some embodiments, the anti-Aβ protofibril antibody comprises a heavy chain comprising an amino acid sequence of SEQ ID NO: 9 and a light chain comprising an amino acid sequence of SEQ ID NO: 10. “CDRs” used herein in the context of an antibody sequence or structure refers to complementarity determining regions, that provide the main determinants of antigen binding. Generally, the antigen-binding site has six CDRs; three in the VH (HCDR1, HCDR2, HCDR3), and three in the VL (LCDR1, LCDR2, LCDR3). The CDRs may be determined according to the Kabat numbering scheme. which may be determined by according to the Kabat numbering scheme (Kabat et al., Sequences of Proteins of Immunological Interest, 5th Ed. Public Health Service, National Institutes of Health, Bethesda, Md., 1991, hereafter referred to as “Kabat report”). In some embodiments, the at least one anti-Aβ protofibril antibody comprises a human constant region. In some embodiments, the human constant region of the at least one anti-Aβ protofibril antibody comprises a heavy chain constant region chosen from IgG1, IgG2, IgG3, IgG4, IgM, IgA, IgE, and any allelic variation thereof as disclosed in the Kabat report. Any one or more of such sequences may be used in the present disclosure. In some embodiments, the heavy chain constant region is chosen from IgG1 and allelic variations thereof. The amino acid sequence of human IgG1 constant region is known in the art and set out in SEQ ID NO: 11. In some embodiments, the human constant region of the at least one anti-Aβ antibody comprises a light chain constant region chosen from κ-λ-chain constant regions and any allelic variation thereof as discussed in the Kabat report. Any one or more of such sequences may be used in the present disclosure. In some embodiments, the light chain constant region is chosen from κ and allelic variations thereof. The amino acid sequence of human κ chain constant region is known in the art and set out in SEQ ID NO: 12. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401, also known as lecanemab. The terms “BAN2401” and “lecanemab” are used interchangeably and refer to a humanized IgG1 monoclonal version of mAb158, which is a murine monoclonal antibody raised to target protofibrils and disclosed in WO 2007 / 108756 and Journal of Alzheimer’s Disease 43: 575-588 (2015). BAN2401 comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regionsAttorney Docket No.08061.0062-00304 (LCDR1 , LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6 (LCDR3) and is described in WO 2007 / 108756 and in Journal of Alzheimer’s Disease 43:575-588 (2015). BAN2401 comprises (i) a heavy chain variable region comprising the amino acid sequence of SEQ ID NO: 7 and (ii) a light chain variable region comprising the amino acid sequence of SEQ ID NO: 8. The full length sequences of heavy chain and light chain of BAN2401 are set forth in SEQ ID NOs: 9 and 10 and are described in WO 2007 / 108756 and in Journal of Alzheimer’s Disease 43:575-588 (2015). In some embodiments, the isolated anti-Aβ protofibril antibody to be used in treatment is present in a concentration of at least 80 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration of at least 100 mg / mL. In some embodiments, the isolated anti- Aβ protofibril antibody is present in a concentration of at least 200 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration of at least 250 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration ranging from 80 mg / mL to 300 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 85 mg / mL to 275 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 90 mg / mL to 250 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 95 mg / mL to 225 mg / mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 100 mg / mL to 200 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 80 mg / mL, 90 mg / mL, 100 mg / mL, 110 mg / mL, 120 mg / mL, 130 mg / mL, 140 mg / mL, 150 mg / mL, 160 mg / mL, 170 mg / mL, 180 mg / mL, 190 mg / mL, 200 mg / mL, 210 mg / mL, 220 mg / mL, 230 mg / mL, 240 mg / mL, 250 mg / mL, 260 mg / mL, 270 mg / mL, 280 mg / mL, 290 mg / mL, or 300 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 100 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 200 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 250 mg / mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 300 mg / mL. In some embodiments, the isolated antibody or fragment thereof is BAN2401. As used herein, a “fragment” of an antibody comprises a portion of the antibody, for example comprising an antigen- binding or a variable region thereof. Non-limiting examples of fragments include Fab fragments, Fab' fragments, F(ab')2 fragments, Fv fragments, diabodies, linear antibodies, and single-chain antibody molecules. 12. Therapeutically effective amount of at least one anti-Aβ protofibril antibody In various embodiments, the methods of the present disclosure comprise administering to a subject a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibrilAttorney Docket No.08061.0062-00304 antibody. As used herein, the term a “therapeutically effective amount” refers to an amount of a compound or pharmaceutical composition sufficient to produce a desired therapeutic effect. One of ordinary skill in the art will understand that the therapeutically effective amount of the at least one anti-Aβ protofibril antibody administered to a subject may depend upon a number of factors including pharmacodynamic characteristics, route of administration, frequency of treatment, and health, age, and weight of the subject to be treated and, with the information disclosed herein, will be able to determine the appropriate amount for each subject. In some embodiments, the therapeutically effective amount is a dose chosen to improve efficacy and / or maintain efficacy and improve at least one of safety and tolerability. In some embodiments, the therapeutically effective amount is chosen to lower at least one side effect and simultaneously improve efficacy and / or maintain efficacy. Therapeutically effective doses of an anti- Aβ protofibril antibody and methods for measuring treatment efficacy are disclosed in PCT / US2022 / 073576; PCT / US2022 / 079571; and PCT / US2022 / 041926 and are incorporated herein by reference. In some embodiments, 0.5 mg / kg to 45 mg / kg, 0.5 mg / kg to 40 mg / kg, 0.5 mg / kg to 35 mg / kg, 0.5 mg / kg to 30 mg / kg, 0.5 mg / kg to 25 mg / kg, 0.5 mg / kg to 20 mg / kg, 0.5 mg / kg to 15 mg / kg, 0.5 mg / kg to 10 mg / kg, 0.5 mg / kg to 5 mg / kg, or 0.5 mg / kg to 2.5 mg / kg of at least one anti- Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg to 45 mg / kg, 2.5 mg / kg to 40 mg / kg, 2.5 mg / kg to 35 mg / kg, 2.5 mg / kg to 30 mg / kg, 2.5 mg / kg to 25 mg / kg, 2.5 mg / kg to 20 mg / kg, 2.5 mg / kg to 15 mg / kg, 2.5 mg / kg to 10 mg / kg, or 2.5 mg / kg to 5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg to 45 mg / kg, 5 mg / kg to 40 mg / kg, 5 mg / kg to 35 mg / kg, 5 mg / kg to 30 mg / kg, 5 mg / kg to 25 mg / kg, 5 mg / kg to 20 mg / kg, 5 mg / kg to 15 mg / kg, or 5 mg / kg to 10 mg / kg, of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg / kg to 45 mg / kg, 7.5 mg / kg to 40 mg / kg, 7.5 mg / kg to 35 mg / kg, 7.5 mg / kg to 30 mg / kg, 7.5 mg / kg to 25 mg / kg, 7.5 mg / kg to 20 mg / kg, 7.5 mg / kg to 15 mg / kg, or 7.5 mg / kg to 10 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, from 0.5 mg / kg, 1 mg / kg, 2 mg / kg, 3 mg / kg, 4 mg / kg, 5 mg / kg, 6 mg / kg, 7 mg / kg, 8 mg / kg, 9 mg / kg, 10 mg / kg, 11 mg / kg, 12 mg / kg, 13 mg / kg, 14 mg / kg, 15 mg / kg, 16 mg / kg, 17 mg / kg, 18 mg / kg, 19 mg / kg, 20 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, up to 20Attorney Docket No.08061.0062-00304 mg / kg, 19 mg / kg, 18 mg / kg, 17 mg / kg, 16 mg / kg, 15 mg / kg, 14 mg / kg, 13 mg / kg, 12 mg / kg, 11 mg / kg, 10 mg / kg, 9 mg / kg, 8 mg / kg, 7 mg / kg, 6 mg / kg, 5 mg / kg, 4 mg / kg, 3 mg / kg, 2 mg / kg, 1 mg / kg, or 0.5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 0.5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 1 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 3 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 4 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 6 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 8 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 9 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 11 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 12 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 12.5 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 13 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 14 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 15 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 16, 17, 18, 19, or 20 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 21, 22, 23, 24, or 25 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject.Attorney Docket No.08061.0062-00304 In some embodiments, 27.5 mg / kg, 30 mg / kg, 32.5 mg / kg, 35 mg / kg, 37.5 mg / kg, 40 mg / kg, 42.5 mg / kg, 45 mg / kg, 47.5 mg / kg, or 50 mg / kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. As mentioned, in some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. Accordingly, in some embodiments, 0.5 mg / kg to 45 mg / kg, 0.5 mg / kg to 40 mg / kg, 0.5 mg / kg to 35 mg / kg, 0.5 mg / kg to 30 mg / kg, 0.5 mg / kg to 25 mg / kg, 0.5 mg / kg to 20 mg / kg, 0.5 mg / kg to 15 mg / kg, 0.5 mg / kg to 10 mg / kg, 0.5 mg / kg to 5 mg / kg, or 0.5 mg / kg to 2.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg to 45 mg / kg, 2.5 mg / kg to 40 mg / kg, 2.5 mg / kg to 35 mg / kg, 2.5 mg / kg to 30 mg / kg, 2.5 mg / kg to 25 mg / kg, 2.5 mg / kg to 20 mg / kg, 2.5 mg / kg to 15 mg / kg, 2.5 mg / kg to 10 mg / kg, or 2.5 mg / kg to 5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg to 45 mg / kg, 5 mg / kg to 40 mg / kg, 5 mg / kg to 35 mg / kg, 5 mg / kg to 30 mg / kg, 5 mg / kg to 25 mg / kg, 5 mg / kg to 20 mg / kg, 5 mg / kg to 15 mg / kg, or 5 mg / kg to 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg / kg to 45 mg / kg, 7.5 mg / kg to 40 mg / kg, 7.5 mg / kg to 35 mg / kg, 7.5 mg / kg to 30 mg / kg, 7.5 mg / kg to 25 mg / kg, 7.5 mg / kg to 20 mg / kg, 7.5 mg / kg to 15 mg / kg, or 7.5 mg / kg to 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, from 0.5 mg / kg, 1 mg / kg, 2 mg / kg, 3 mg / kg, 4 mg / kg, 5 mg / kg, 6 mg / kg, 7 mg / kg, 8 mg / kg, 9 mg / kg, 10 mg / kg, 11 mg / kg, 12 mg / kg, 13 mg / kg, 14 mg / kg, 15 mg / kg, 16 mg / kg, 17 mg / kg, 18 mg / kg, 19 mg / kg, 20 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, up to 20 mg / kg, 19 mg / kg, 18 mg / kg, 17 mg / kg, 16 mg / kg, 15 mg / kg, 14 mg / kg, 13 mg / kg, 12 mg / kg, 11 mg / kg, 10 mg / kg, 9 mg / kg, 8 mg / kg, 7 mg / kg, 6 mg / kg, 5 mg / kg, 4 mg / kg, 3 mg / kg, 2 mg / kg, 1 mg / kg, or 0.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 0.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 1 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 3 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 4 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg of BAN2401 is administered to the subject relative to bodyAttorney Docket No.08061.0062-00304 weight of the subject. In some embodiments, 6 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 8 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 9 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 11 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 12 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 12.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 13 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 14 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 15 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 16, 17, 18, 19, or 20 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 21, 22, 23, 24, or 25 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 27.5 mg / kg, 30 mg / kg, 32.5 mg / kg, 35 mg / kg, 37.5 mg / kg, 40 mg / kg, 42.5 mg / kg, 45 mg / kg, 47.5 mg / kg, or 50 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg to 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg to 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg / kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, a subject is administered a first dose of the anti-Aβ protofibril antibody without an initial titrating step up to the treatment dose (e.g., a subject starts treatment at 10 mg / kg with no titration). In some embodiments, a dose of BAN2401 may be used without the need of a prior titrating step. In some embodiments, a subject is switched to a maintenance dose without an initial titrating step to the maintenance dose. In certain instances, providing a therapeutic dose without a titration step may provide additional therapeutic benefits to the patient, e.g., a faster shift in plasma biomarkers toward amyloid negativity or facilitating identification sooner of patients that do not have a therapeutic change in plasma biomarkers in response to the anti-Aβ protofibril antibody (non- responders) and who would benefit from alternative treatment.Attorney Docket No.08061.0062-00304 13. Dosage Regimens and Routes of Administration In various embodiments, methods are disclosed herein for treating AD that comprise administration of an anti-Aβ protofibril antibody (e.g., BAN2401) to a subject. In some embodiments, the subject has early AD. In some embodiments, a subject who has pre-AD or is suspected of having AD is administered an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, the anti- Aβ protofibril antibody may be administered to a subject according to a dosage regimen (also called a “dosing regimen,” “treatment regimen” or “treatment,”), e.g., a schedule specifying doses of the anti- Aβ protofibril antibody administered per unit of time, including the number of doses over a given time period and the elapsed time between doses. In some embodiments, the dosage regimen comprises administering the anti-Aβ protofibril antibody at a specified dose, according to a schedule (e.g., on a repetitive basis). In some embodiments, the anti-Aβ protofibril antibody may be administered daily, once weekly, also called “weekly”, or every other week, also called “biweekly”, or monthly, also called “every 4 weeks.” In some embodiments, the anti-Aβ protofibril antibody may be administered intravenously and / or subcutaneously. In some embodiments, a dosage regimen comprises administration of at least one initiation dose (also called a treatment dose) and at least one maintenance dose. In some embodiments, the dosing regimen comprises administration of at least one dose of the anti-Aβ protofibril antibody via one route of administration. In some embodiments, the dosing regimen comprises administration of at least one dose of the anti-Aβ protofibril antibody via more than one route of administration (e.g., initially administering an antibody intravenously and then switching to subcutaneous administration). In some embodiments, the anti-Aβ protofibril antibody is administered intravenously, e.g., by an injection into a peripheral vein. In an upper extremity, the median basilic or cephalic veins of the arm or the metacarpal veins in the hand’s dorsum may be used. In a lower extremity, the dorsal venous plexus of the foot may be used. After 18 months, population modeling predicts that reducing the frequency of 10 mg / kg to once every 4 weeks will continue the reduction in amyloid beta plaque levels. In some embodiments, the anti-Aβ protofibril antibody is administered subcutaneously. In a subcutaneous injection, the anti-Aβ protofibril antibody is injected into the tissue layer between the skin and muscle, such as a fatty tissue just below the skin. In some embodiments, the subcutaneous administration is injected into the abdomen (e.g., at or under the level of the belly button), thigh (e.g., front of the thigh), or upper arm (e.g., back or side of the upper arm). In some embodiments, a volume of the injection administered subcutaneously is less than 2 mL. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered using a vial and syringe (also called “vial / syringe” or “syringe / vial” or “SC Vial”). For example, theAttorney Docket No.08061.0062-00304 anti-Aβ protofibril antibody in a subcutaneous formulation may be removed from a vial into a syringe and then injected from the syringe into the subject. In some embodiments, the anti-Aβ protofibril antibody is administered using an autoinjector (also called an “auto-injector,” “AI,” “AI Device,” or “SC AI”). An exemplary auto- injector is the YpsoMate™ 2.25 mL AI Device, which has been approved in the United States (US) and Europe as a presentation for Ajovy® (fremanezumabv-frm). In some embodiments, an autoinjector may comprise a plastic PLAJEX™ syringe, a tapered needle (24G-29G), a V spring, a spring force, and component colors. It may be a single-use, disposable injection device consisting of a housing with a content viewing window, a spring activated mechanism, and integrated needle safety feature. In some embodiments, a 2.25 mL PLAJEX™ syringe may be prefilled with the anti-Aβ protofibril antibody. At least one AI Device may be needed to administer the dose of the anti-Aβ protofibril antibody. In some embodiments, the anti-Aβ protofibril antibody is administered intravenously for at least one dose, and subcutaneously for at least one dose. For example, the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered to a subject intravenously, e.g., once weekly, for a period of time, such as 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, or 24 months, after which the antibody may be administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody may be administered subcutaneously using a vial-syringe, and then later administered subcutaneously using an AI. In some embodiments, the anti-Aβ protofibril antibody may be administered subcutaneously using a vial-syringe or an AI, and then later administered intravenously. In some embodiments, the method of treatment comprises switching between an intravenous or subcutaneous dose, or from an initiation to a maintenance dose, at a set time point (e.g., after 18 months or after 24 months). In some embodiments, the method of treatment comprises using a biomarker level to determine switching between an intravenous or subcutaneous dose or from an initiation to a maintenance dose, e.g., when measured at or after a set time point (e.g., after 18 months or after 24 months). In some embodiments, a maintenance dose is administered subcutaneously (e.g., as one or more subcutaneous injections). In some embodiments, BAN2401 (also called LEQEMBI, lecanemab, or lecanemab-irmb) is supplied as a solution for intravenous use and is a preservative-free, sterile, clear to opalescent and colorless to pale yellow solution for intravenous use by infusion after dilution. In some embodiments, LEQEMBI may be supplied in single-dose vials available in concentration of 500 mg / 5 mL (100 mg / mL) or 200 mg / 2 mL (100 mg / mL). In some embodiments, each mL of solution contains 100 mg of lecanemab-irmb and arginine hydrochloride (42.13 mg), histidine (0.18 mg), histidine hydrochloride monohydrate (4.99 mg), polysorbate 80 (0.50 mg), and Water for Injection at an approximate pH of 5.0. In some embodiments, LEQEMBI is diluted in 250 mL of 0.9% SodiumAttorney Docket No.08061.0062-00304 Chloride Injection, USP. In some embodiments, a dosage of LEQEMBI is 10 mg / kg, relative to the weight of the subject. a. Initiation Doses In some embodiments, the anti-Aβ protofibril antibody may be administered to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) according to a dosage regimen (also called a dosing regimen) in which a dose, e.g., a therapeutically effective dose, is administered at a regular dosing interval on a repetitive basis. In some embodiments, the dose may be called an initiation dose, a treatment dose, or a first dose. The initiation dose may be administered to a subject according to a dosage regimen (e.g., an initiation dosage regimen, also called an initiation dosing regimen) in which initiation dose of the anti-Aβ protofibril antibody may be administered at an interval (e.g., daily, weekly, biweekly, or monthly), for a period of time, e.g., until the subject shows evidence of improved AD pathology and / or slowed progression of AD. In some embodiments, the period of time is at least 18 months or at least 24 months. In some embodiments, the period of time is 18 months. In some embodiments, the period of time is 24 months. In some embodiments, the period of time is about 12 months, 18 months, 24 months, 30 months, 36 months, 42 months, 48 months, 54 months, or 60 months. In some embodiments, the initiation dose may be administered until the subject is amyloid negative. In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody is administered intravenously to the subject. An exemplary dosage regimen may comprise intravenously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 10 mg / kg. In some embodiments, BAN2401 is administered intravenously, once weekly, at a dose of 10 mg / kg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative or until one or more other biomarker levels are reached (e.g. a change in a biomarker discussed herein). In some embodiments, BAN2401 is administered intravenously, biweekly, at a dose of 10 mg / kg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g. a change in a biomarker discussed herein). In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is administered subcutaneously, e.g., by vial-syringe or by autoinjector. An exemplary dosage regimen may comprise subcutaneously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 720 mg. In some embodiments, the dose may be administered in one single injection of 720 mg. In some embodiments, the dose of 720 mg may be administered in two concurrent, e.g., sequential, injections of 360 mg (e.g., 2 x 1.8 mL of 400 mg / 2 mL or 2 x 1.8 mL of 200 mg / mL). In some embodiments, BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for 18 months. In some embodiments, BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for 24 months. In some embodiments,Attorney Docket No.08061.0062-00304 BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g., a change in a biomarker discussed herein). In some embodiments, BAN2401 is administered subcutaneously, biweekly, at a dose of 720 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g., a change in a biomarker discussed herein). The dose of 720 mg may be administered in two concurrent, e.g., sequential, injections of 360 mg (e.g., 2 x 1.8 mL of 400 mg / 2 mL or 2 x 1.8 mL of 200 mg / mL). In some embodiments, different initiation doses of the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered. In some embodiments, a subcutaneous dose of the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered at more than one dose. For example, a subject may be transitioned from a first dose of the antibody for a first period of time to a second dose of the antibody for a second period of time. For example, a dose of 720 mg may be administered subcutaneously, once weekly, for a first period of time, after which a dose of 500 mg may be administered subcutaneously, once weekly, for a second period of time. In some embodiments, the 720 mg dose is administered in 2 consecutive injections of 360 mg (2x1.8 mg of 200 mg / mL subcutaneous formulation) for the first period of time, and then the 500 mg dose is administered in 2 consecutive injections of 250 mg (2x1.25 mL of 200 mg / mL subcutaneous formulation) for the second period of time. In some embodiments, the first period of time is less than about 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, or 24 months, or less than a period of time until the subject is amyloid negative, or one or more biomarker levels as discussed herein are reached. In some embodiments, the first period of time is less than 18 months. In some embodiments, the second period comprises the first period of time plus the remainder of 18 months, so that the first and second time periods are about 18 months in total. In some embodiments, a subject may receive the subcutaneous dose of 720 mg of the anti-Aβ protofibril antibody (e.g., BAN2401) weekly, via an autoinjector, for a first period of time, and then a subcutaneous dose of 500 mg of the anti-Aβ protofibril antibody (e.g., BAN2401) weekly, via an autoinjector, for a second period of time. In some embodiments, an initiation dosing regimen of the Aβ protofibril antibody (e.g., BAN2401) may comprise administration of the antibody at more than one dose and / or via more than one mode of administration. In some embodiments, a subject may be transitioned from a first dose of the antibody, administered intravenously, for a first period of time, to a second dose of the antibody, administered either intravenously or subcutaneously, for a second period of time. In some embodiments, the subject may be transitioned from a first dose of the antibody, administered intravenously, for a first period of time, to a second dose of the antibody, administered subcutaneously, for a second period of time. For example, a first dose of 10 mg / kg may be administered to the subject intravenously, biweekly, for at first period of time (e.g., 6 months or 12Attorney Docket No.08061.0062-00304 months), after which a second dose of 720 mg or less (e.g., 500 mg) maybe administered for a second period of time (e.g., 6 months or 12 months). In some embodiments, the initiation dosage regimen comprising a first dose of the Aβ protofibril antibody (e.g., BAN2401) administered intravenously a first period of time, and a second dose of the Aβ protofibril antibody administered subcutaneously for a second period of time may be followed by a maintenance dosing regimen, such as a maintenance dosing regimen comprising subcutaneous administration of the antibody at a dose of 360 mg biweekly, or subcutaneous administration of the antibody at a dose of 250 mg biweekly. In some embodiments, a subject’s exposure to an anti-Aβ protofibril antibody depends on whether the dose was administered using a vial / syringe or an AI. In some embodiments, exposure to the antibody when using an AI is greater than when using a vial / syringe. Accordingly, the dose subcutaneously administered using an AI may be lower than a dose subcutaneously administered using a vial / syringe. In some embodiments, where a target systemic exposure is based on an intravenous administration (e.g., 10 mg / kg biweekly), the exposure from the dose subcutaneously administered using an AI method may be higher than that obtained using a vial / syringe method. Accordingly, the dose administered subcutaneously using an AI may be lower than a dose administered subcutaneously using a vial / syringe. In some embodiments, the systemic exposure from a dose intravenously administered at 10 mg / kg biweekly is about equal to a dose subcutaneously administered at 720 mg weekly using a vial / syringe method, or to a dose subcutaneously administered at 500 mg weekly using an AI method. For example, the dosage of the anti-Aβ protofibril antibody subcutaneously administered using an AI method may be about 40%, 45%, 50%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, or 95% of the dosage subcutaneously administered using a vial / syringe method. In some embodiments, the dosage of the anti-Aβ protofibril antibody subcutaneously administered using an AI method 65%, 66%, 67%, 68%, 69%, or 70% of the dose subcutaneously administered using a vial / syringe method. In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is administered subcutaneously by autoinjector (AI). An exemplary dosage regimen may comprise subcutaneously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 500 mg, e.g., using an AI. The dose of 500 mg may be administered in a single injection of 500 mg. The dose of 500 mg may be administered in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg / 2 mL, which is also 2 x 1.25 mL of 200 mg / mL). In some embodiments, BAN2401 is administered subcutaneously using an AI, once weekly, at a dose of 500 mg for 18 months. In some embodiments, BAN2401 is administered subcutaneously using an AI, once weekly, at a dose of 500 mg for 24 months. In some embodiments, BAN2401 is administered subcutaneously using an AI, biweekly, at a dose of 500 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative. In some embodiments, BAN2401 is administered subcutaneously using an AI, biweekly, at a dose of 500 mg, e.g., for at least 18 months or at least 24Attorney Docket No.08061.0062-00304 months, or e.g., until the subject is amyloid-negative. The dose of 500 mg may be administered in a single injection of 500 mg. The dose of 500 mg may be administered in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg / 2 mL or 2 x 1.25 mL of 200 mg / mL). In some embodiments, at least one of the dose, frequency of administration, or mode of administration of the anti-Aβ protofibril antibody may be selected and / or changed to achieve a target systemic exposure (e.g., AUC) to the antibody. In some embodiments, a target systemic exposure is the same regardless of the mode of administration. For example, an exemplary target systemic exposure may be achieved when the anti-Aβ protofibril antibody is intravenously administered at 10 mg / kg biweekly. The same target systemic exposure may be achieved when the anti-Aβ protofibril antibody is subcutaneously administered at 720 mg, e.g., weekly. In some embodiments, the same target systemic exposure may be achieved when the anti-Aβ protofibril antibody is subcutaneously administered at 500 mg, e.g., weekly. In some embodiments, a patient first receives the anti-Aβ protofibril antibody (e.g., BAN2401) intravenously administered at 10 mg / kg dose, and later receives the antibody subcutaneously administered at a dose (e.g., 720 mg weekly or 500 mg weekly) that achieves about the same target systemic exposure as the intravenous dose. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg weekly) selected to achieve a target systemic exposure calculated to be equivalent to that achieved by intravenous administration at 10 mg / kg biweekly, whether or not the patient has previously received an intravenous administration of the antibody. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg) weekly. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose of 500 mg weekly. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg) biweekly.In some embodiments, administering a low dose of the anti-Aβ protofibril antibody (e.g., in an initiation dose) or reducing the dose (e.g., in either an initiation dose or in a subsequent maintenance dose) may lower or reduce the patient’s risk for developing ARIA, while still retaining the ability to improve AD pathology or slow progression of AD. For example, the dose of the anti-Aβ protofibril antibody may be reduced by lowering the dose in each administration, reducing the frequency of administration, or changing the method of administration. The reduced dose may be adequate to clear Aβ and reduce or slow one or more of tau aggregation, expression of biomarkers of AD, cognitive decline, and / or indicators of AD pathology. In another example, a patient may be on a treatment dose and then moved, e.g., after 18 months or after 24 months of treatment, to a maintenance dose that is lower or administered less frequently while stabilizing or continuing to see reduced levels of brain Aβ protofibril, e.g., as measured by continued changes in amyloid PET scans and / or one or more biomarkers of amyloid.In some embodiments, the subject has AD, is suspected of having AD, or is at risk for AD. In some embodiments, the subject has AD, e.g., early AD. In some embodiments, the subject has pre-AD.Attorney Docket No.08061.0062-00304 b. Maintenance Doses In some embodiments, a maintenance dose of the anti-Aβ protofibril antibody may be administered to the subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD). The maintenance dose may be a dose administered to maintain therapeutically effective concentrations of the anti-Aβ protofibril antibody in the subject and / or to maintain or continue to reduce levels of Aβ protofibril in the brain of the treated subject. Without being bound by theory, it has been found by the inventors that after an initiation regimen of an anti-Aβ protofibril antibody such as BAN2401 in a subject, a maintenance dosing regimen may be administered at a reduced frequency or dosage, or a different route of administration, while holding level or continuing to reduce Aβ protofibrils in the brain. In some embodiments, the maintenance dose may be administered to a subject according to a dosage regimen (e.g., a maintenance dosage regimen, also called a maintenance dosing regimen) in which the maintenance dose is administered at a regular interval on a repetitive basis. In some embodiments, each maintenance dose of the anti-Aβ protofibril antibody may be administered daily, weekly, biweekly, or monthly. Administering at least one maintenance dose of the anti-Aβ protofibril antibody, e.g., according to a maintenance regimen which succeeds a treatment regimen, may prevent a return to baseline (e.g., pretreatment) levels of markers of AD pathology. For example, when a treatment regimen is stopped or interrupted, amyloid PET may rebound and / or plasma biomarkers, e.g., the p- tau181 levels and the Aβ42 / 40 ratio, may return to baseline pre-treatment levels. This effect has been corroborated by predicted rates of early amyloid reaccumulation based on data from gantenerumab and donanemab, as well as observations from a gap period in Study 201, a multicenter, double-blind, placebo-controlled, Phase 2b trial conducted in 856 patients with early AD. A core study in Study 201 evaluated key efficacy assessments, including clinical change on the AD Composite Score (ADCOMS) as the primary endpoint at 12 months and as key secondary endpoints, ADCOMS, Clinical Dementia Rating-Sum-of-Boxes (CDR-SB) and AD Assessment Scale-Cognitive Subscale 14 (ADAS-Cog14) at 18 months. Following analysis of the 18-month core phase, an intervening off- treatment period (gap period) ranging from 9-59 months (mean 24 months) was taken, which was followed by an OLE with 10 mg / kg IV bi-weekly lecanemab dosing to assess long-term safety and tolerability. Subjects who stopped treatment showed an increase in amyloid PET by approximately 7 Centiloids (21% return to pretreatment baseline) and an increase in p-tau181 and the Aβ42 / 40 ratio indicating return of 24%, and 47%, respectively, to pre-treatment baseline levels. Thus, in some embodiments, continued treatment with at least one maintenance dose of the anti-Aβ protofibril antibody may maintain suppression of the disease progression rate and / or prevent reaccumulation of AD pathology which may occur if treatment is stopped.Attorney Docket No.08061.0062-00304 In some embodiments, a maintenance dose may be administered after a preset time period, e.g., after completion of an initiation dosage regimen. For example, a maintenance dose may be administered after about 18 months of treatment with an initiation dose, or the maintenance dose may be administered after about 24 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 30 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 36 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 48 months of treatment with an initiation dose. In some embodiments, the maintenance dose may be the same as the initiation dose. In some embodiments, a maintenance dose may be lower than the initiation dose. In some embodiments, a maintenance dose may be administered less frequently than the initiation dose. This may reduce the burden for subjects and their caregi...

Claims

Attorney Docket No.08061.0062-00304 CLAIMS 1. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3).

2. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences 3. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3).

4. A method of converting an amyloid positive subject to amyloid negative, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3).

5. The method of any one of claims 1-4, wherein the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and / or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously.Attorney Docket No.08061.0062-00304 6. The method of any one of claims 1-5, wherein the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously.

7. The method of any one of claims 1-6, wherein the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg.

8. The method of any one of claims 1-7, wherein the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg.

9. The method of any one of claims 1-8, wherein the dose is administered in two parts, e.g., consecutively.

10. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once weekly.

11. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once biweekly.

12. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once monthly.

13. The method of any one of claims 1-12, wherein the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen.

14. The method of claim 13, wherein the initiation dosing regimen comprises intravenous administration of each initiation dose or subcutaneous administration of each initiation dose.

15. The method of claim 13 or claim 14, wherein the maintenance dosing regimen comprises subcutaneous administration of each maintenance dose or intravenous administration of each maintenance dose.

16. The method of claim 13 or claim 15, wherein the initiation dosing regimen comprises at least one initiation dose administered intravenously and at least one initiation dose administered subcutaneously.

17. The method of any one of claims 13, 14, or 16, wherein the maintenance dosing regimen comprises at least one maintenance dose administered intravenously and at least one maintenance dose administered subcutaneously.Attorney Docket No.08061.0062-00304 18. The method of any one of claims 13-17, wherein the initiation dose is greater than the maintenance dose.

19. The method of claim 13, wherein the initiation dose of the anti-Aβ protofibril antibody is 150 mg to 600 mg, e.g., 200 mg to 550 mg, preferably 500 mg, administered subcutaneously.

20. The method of claim 13, wherein the maintenance dose of the anti-Aβ protofibril antibody is 150 mg to 500 mg, e.g., 360 mg, administered subcutaneously.

21. The method of claim 20, wherein the maintenance dose of the anti-Aβ protofibril antibody is 250 mg administered subcutaneously.

22. The method of any one of claims 13-21, wherein the initiation dose is administered weekly.

23. The method of any one of claims 13-22, wherein the maintenance dose is administered weekly.

24. The method of any one of claims 13-22, wherein the maintenance dose is administered biweekly.

25. The method of any one of claims 13-24, wherein the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months.

26. The method of claim 25, wherein the first time period is at least 18 months.

27. The method of claim 25 or claim 26, wherein the first time period is at least 24 months.

28. The method of any one of claims 13-27, wherein the first time period lasts until the subject is amyloid negative.

29. The method of claim 13, wherein the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time.

30. The method of claim 13, wherein the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 24 months, and then subcutaneously administered at a maintenance dose of 250 mg biweekly for the second period of time.

31. The method of any one of claims 13-30 wherein the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression.

32. The method of any one of claims 13-31, wherein the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject.

33. The method of any one of claims 13-32, wherein the maintenance dose is subcutaneously administered with an autoinjector (AI).Attorney Docket No.08061.0062-00304 34. The method of any one of claims 13-17, wherein the anti-Aβ protofibril antibody is intravenously administered at a dose of 10 mg / kg relative to the weight of the subject, biweekly.

35. The method according to any one of claims 1-34, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe.

36. The method according to any one of claims 1-34, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition via an autoinjector.

37. The method according to any one of claims 1-36, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO:

2.

38. The method according to any one of claims 1-37, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab).

39. The method of any one of claims 1-38, wherein the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment.

40. The method of claim 39, wherein the change and / or difference in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42 / 1-40 and / or increased total tau, p- tau (e.g., p-tau181, p-tau217, and / or p-tau231), the ratio of p-tau181 / np-tau181, the ratio of p- tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL).

41. The method of any one of claims 1-38, wherein the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology during and / or after treatment.

42. The method of claim 40, wherein the change and / or difference in the measurement is selected from:Attorney Docket No.08061.0062-00304 a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42 / 1-40 and / or decreased total tau, p- tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p-tau181 / np-tau181, the ratio of p- tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL).

43. The method of any one of claims 1-42, wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), a CSF assessment of total tau, a CSF assessment of p-tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np-tau217), MRI, retinal amyloid accumulation, and / or a blood biomarker assessment (e.g. a plasma Aβ1-42 / 1-40 ratio, plasma p-tau181, plasma p- tau217, plasma p-tau 231 level, the ratio of p-tau181 / np-tau181, and / or the ratio of p-tau217 / np- tau217).

44. The method according to any one of claims 1-43, wherein the subject is ApoE4-positive.

45. The method of any one of claims 1-44, wherein the subject is monitored for development of ARIA.

46. The method any one of claims 1-45, wherein the subject is 65 to 80 years old.

47. The method any one of claims 1-45, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration.

48. The method of any one of claims 1-47, wherein the subject has Alzheimer’s disease.

49. The method of any one of claims 1-48, wherein the subject has early Alzheimer’s disease.

50. The method of any one of claims 1-49, wherein the subject has been diagnosed withAttorney Docket No.08061.0062-00304 a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment.

51. The method of any one of claims 1-47, wherein the subject is suspected of having AD.

52. The method of any one of claims 1-47, wherein the subject is a subject at risk for developing AD.

53. The method of claim 52, wherein the subject at risk for developing AD has pre-AD.

54. The method of claim 52 or claim 53, wherein the subject does not have cognitive impairment.

55. The method of any one of claims 52-54, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration.

56. The method of any one of claims 52-55, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration.

57. The method of any one of claims 52-56, wherein the subject has a Wechsler Memory Scale- Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years.

58. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibodyAttorney Docket No.08061.0062-00304 comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

59. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

60. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

61. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chainAttorney Docket No.08061.0062-00304 complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg / kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

62. The method of any one of claims 58-61, wherein the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months.

63. The method of any one of claims 58-62, wherein the initiation dose of the antibody is administered intravenously for at least 18 months.

64. The method of any one of claims 58-63, wherein the initiation dose of the antibody is administered intravenously for at least 24 months.

65. The method of any one of claims 58-64, wherein the maintenance dose of the antibody is administered weekly.

66. The method of any one of claims 58-64, wherein the maintenance dose of the antibody is administered biweekly.

67. The method of any one of claims 58-66, wherein the maintenance dose of the antibody is administered using a vial-syringe.

68. The method of any one of claims 58-66, wherein the maintenance dose of the antibody is administered using an AI.

69. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; andAttorney Docket No.08061.0062-00304 subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

70. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

71. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.

72. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg.Attorney Docket No.08061.0062-00304 73. The method of any one of claims 69-72, wherein the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months.

74. The method of any one of claims 69-73, wherein the initiation dose of the antibody is administered subcutaneously for at least 18 months.

75. The method of any one of claims 69-73, wherein the initiation dose of the antibody is administered subcutaneously for at least 24 months.

76. The method of any one of claims 69-75, wherein the initiation dose of the antibody is administered using a vial-syringe.

77. The method of any one of claims 69-76, wherein the initiation dose of the antibody is administered using an AI.

78. The method of any one of claims 69-77, wherein the maintenance dose of the antibody is administered weekly.

79. The method of any one of claims 69-77, wherein the maintenance dose of the antibody is administered biweekly.

80. The method of any one of claims 69-79, wherein the maintenance dose of the antibody is administered using a vial-syringe.

81. The method of any one of claims 69-79, wherein the maintenance dose of the antibody is administered using an AI.

82. The method according to any one of claims 69-81, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO:

2.

83. The method according to any one of claims 69-82, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab).

84. The method of any one of claims 69-83, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment.

85. The method of claim 84, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET),Attorney Docket No.08061.0062-00304 c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42 / 1-40, and / or increased total tau, p- tau (e.g, p-tau181, p-tau217, and / or p-tau231), ratio of p-tau181 / np-tau181, ratio of p-tau217 / np- tau217, neurogranin, and / or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231, ratio of p- tau181 / np-tau181, ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL).

86. The method of any one of claims 69-84, wherein the subject shows a change and / or difference in a measurement of one or more biomarkers associated with AD pathology during and / or after treatment.

87. The method of claim 86, wherein the change and / or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42 / 1-40 and / or decreased total tau, p- tau (e.g., p-tau181, p-tau217, and / or p-tau231, the ratio of p-tau181 / np-tau181, and / or the ratio of p- tau217 / np-tau217), neurogranin, and / or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42 / 1-40 and / or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and / or P-tau231), ratio of p- tau181 / np-tau181, the ratio of p-tau217 / np-tau217, glial fibrillary acidic protein (GFAP), and / or neurofilament light chain (NfL).

88. The method of any one of claims 58-87 wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation.

89. The method according to any one of claims 58-88, wherein the subject is ApoE4-positive.

90. The method of any one of claims 58-89, wherein the subject is monitored for development of ARIA.

91. The method any one of claims 58-90, wherein the subject is 65 to 80 years old.

92. The method any one of claims 58-90, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from:Attorney Docket No.08061.0062-00304 (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration.

93. The method of any one of claims 58-93, wherein the subject has Alzheimer’s disease.

94. The method of any one of claims 58-93, wherein the subject has early Alzheimer’s disease.

95. The method of any one of claims 58-94, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and / or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment.

96. The method of any one of claims 58-92, wherein the subject is suspected of having AD.

97. The method of any one of claims 58-92, wherein the subject is a subject at risk for developing AD.

98. The method of claim 97, wherein the subject at risk for developing AD has pre-AD.

99. The method of claim 97 or claim 98, wherein the subject does not have cognitive impairment.

100. The method of any one of claims 97-99, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration.

101. The method of any one of claims 97-100, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration.Attorney Docket No.08061.0062-00304 102. The method of any one of claims 97-101, wherein the subject has a Wechsler Memory Scale- Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years.

103. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg.

104. A method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg.

105. A method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising:Attorney Docket No.08061.0062-00304 administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg.

106. A method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg.

107. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg / kg relative to the weight of the subject; orAttorney Docket No.08061.0062-00304 subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg.

108. The method of any one of claims 103-107, wherein the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe.

109. The method of any one of claims 103-107, wherein the subcutaneously administered maintenance dose of the antibody is administered using an AI.

110. The method of any one of claims 103-109, wherein the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab.

111. The method of claim 110, wherein the first anti-Aβ antibody is donanemab.

112. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg / kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 250 mg.

113. The method of any one of claims 1-112, wherein the subject is on a thrombolytic or anti- platelet agent but not an anticoagulant.

114. The method of claim 113, wherein the subject is receiving an anti-platelet medication.

115. The method of claim 113, wherein the subject is receiving a thrombolytic agent.

116. The method of claim 115, wherein the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent.

117. The method of claim 116, wherein the subject is receiving aspirin.

118. The method of claim 116, wherein the subject is receiving a fibrinolytic.Attorney Docket No.08061.0062-00304 119. The method of any one of claims 1-118, wherein the subject has had or is at an increased risk for a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment.

120. The method of any one of claims 1-118, wherein the subject has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment.

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