Compositions and methods for treating multiple system atrophy (MSA)

Abstract

The present invention relates to methods of treating early multiple system atrophy (MSA) or MSA-C using anti-alpha synuclein antibodies, such as Amlenetug.   

Description

Compositions Methods for treating multiple systemic atrophy ( MSA ) The technical field of invention This invention relates to the clinical uses of antibodies bound to human alpha-synuclein protein for the treatment of synonucleopathies or prodromal synonucleopathy. Reference to the list sequences This request includes a list of one or more sequences deposited in a file in a computer-readable format (filename: "PCT Seq list ST26.xml1294-WO-", created on February 21, 2025, and 58 KB in size), and this file is merged here with its entire contents. Technical background of to invent Cynopathies refer to disorders characterized by the presence of abnormal collections of alpha-synuclein protein within neurons known as Lewy bodies. Cynopathies include Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), diffuse Lewy body disease (DLB) (also known as dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease (CAPD), autonomic nervous system failure (PAF), and multiple system atrophy (MSA; for example, cerebellar olivary atrophy, black striatal degeneration, and Shay-Draeger syndrome). Alpha-synuclein protein (α-synuclein) is naturally associated with synapses and is thought to play a role in regulating synaptic vesicle release, thereby influencing neural communication, neuroplasticity, learning, and memory. Synonucleopathies have been widely associated with α-synuclein aggregations; however, the specific pathogenic α-synuclein species remain unknown. Multiple types of the protein, ranging from oligomers to fibrils, as well as various post-translational modifications, have been implicated in toxicity, but there is no consensus on which species is most important, if indeed there is a single toxic species. The antibodies identified in application WO2017 / 009312 bind to multiple alpha-synuclein isoforms, including all major known variants resulting from alternative splicing or post-translational modifications, such as truncated isoforms, as well as oligomeric and fibrous isoforms. These antibodies are believed to be useful in the treatment and / or diagnosis of alpha-synuclein-related diseases, such as synaptic disorders and / or conditions involving abnormal accumulation or deposition of alpha-synuclein in the central nervous system. Application WO2017 / 009312 also describes the methods for producing these antibodies, as well as their various functional and structural properties. Application WO2023 / 041524 describes specific dosing regimens for administering the antibodies identified in application WO2017 / 009312. Unveiling invention One of the aims of this invention is to provide methods for the clinical use of antibodies directed against alpha-synuclein for the treatment of synonucleopathies or prodromal synonucleopathy. The inventors of this invention developed a method for treating MSA in humans using antibodies targeting alpha-synuclein. Data presented in the experimental section (Example 8 and Figures 12-20) consistently demonstrate the ability of the specific anti-alpha-synuclein antibody, GM37var2, to slow the clinical progression of the disease in MSA patients. In one respect, the invention provides an anti-alpha-synoclane monoclonal antibody for use in the treatment of synoclane disorders or prodromal synoclane disorders, the said use of which involves the intravenous administration of the said anti-alpha-synoclane antibody to a person under treatment who has or is at risk of developing a synoclane disorder, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The said anti-alpha-synoclane monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence Identification Number: 9 (ILEDMP)) of human alpha-synoclane (Sequence Identification Number: 10). In one respect, the invention provides an anti-alpha-synuclein monoclonal antibody for use in the treatment of multiple system atrophy (MSA), whereby the said use involves the intravenous administration of the said anti-alpha-synuclein antibody to a person undergoing treatment who has MSA or is at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The said anti-alpha-synuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). On the other hand, the invention provides a method for treating synonucleopathies or prodromal synonucleopathies. The method involves administering an anti-alpha-synonuclein monoclonal antibody intravenously to a patient in need of treatment, where the person is suffering from or at risk of developing a synonucleopathy, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The anti-alpha-synonuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9) (ILEDMP()) of human alpha-synonuclein (Sequence ID: 10). On the other hand, the invention provides a method for treating MSA. The method involves administering an anti-alpha-synuclein monoclonal antibody intravenously to a person undergoing treatment who needs it, as the person in question has MSA or is at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The aforementioned anti-alpha-synuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9) (ILEDMP) of human alpha-synuclein (Sequence ID: 10). On another side, the invention also provides for the use of an anti-alpha-synoclean monoclonal antibody in the manufacture of a drug for the treatment of synoclean disorders or prodromal synoclean disorders, where the aforementioned use involves the intravenous administration of the said anti-alpha-synoclean antibody to a person under treatment who has or is at risk of developing a synoclean disorder, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The said anti-alpha-synoclean monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence Identification Number: 9 (ILEDMP)) of human alpha-synoclean (Sequence Identification Number: 10). On another side, the invention also provides for the use of an anti-alpha-synoclean monoclonal antibody in the manufacture of a drug for the treatment of synoclean disorders or prodromal synoclean disorders, where the aforementioned use involves the intravenous administration of the aforementioned anti-alpha-synoclean antibody to a person undergoing treatment who has MSA or is at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg. The aforementioned anti-alpha-synoclean monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synoclean (Sequence ID: 10). In one of these aspects, this invention provides clinically appropriate uses for the treatment of syncytia disorders, such as Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, purely autonomic nervous system failure, or multiple system atrophy (MSA), such as probable MSA, likely MSA, type C MSA, type P MSA, clinically confirmed MSA, or clinically probable MSA. In another embodiment of these aspects, this invention provides suitable clinical uses for the treatment of prodromal synopathies in a person undergoing treatment who is at risk of developing a synopathy, such that this person undergoing treatment can be identified by showing one or more clinical signs of prodromal synopathies such as REM rapid eye movement sleep behavior disorder such as isolated RBD (iRBD), olfactory disorder such as hyposmia, abnormal cognitive performance on neuropsychological tests, mild motor dysfunction or abnormal motor performance assessed by objective tests, color vision disorder, autonomic nervous system disorders (such as constipation, urinary symptoms, erectile dysfunction, or orthostatic hypotension), reduced black striatal dopaminergic binding in the pituitary and striatum (abnormal DAT-SPECT), seborrheic dermatitis, or a genotype associated with an increased risk of phenotypic transformation such as mutations in the glucocerebrosidase enzyme (encoded by the GBA gene). In certain embodiments, the invention provides suitable clinical uses for the GM37 monoclonal antibody and its variants, namely GM37 Variant 1, GM37 Variant 2, and GM37 Variant 3, the composition, methods, and properties of which are all disclosed in application WO2017 / 009312. In certain embodiments of these aspects, the monoclonal antibody directed against alpha-synuclein and intended for use according to the invention is given once every 3-5 weeks, such as approximately once every 4 weeks, or once a month, such as every 28-30 days. In certain embodiments of these aspects, the monoclonal antibody directed against alpha-synuclein and intended for use according to the invention is given at a dose of approximately 750 mg, or approximately 1050 mg, or approximately 1400 mg, or approximately 1750 mg, or approximately 2100 mg, or approximately 2450 mg, or approximately 2800 mg, or approximately 3150 mg, or approximately 3500 mg, or approximately 3850 mg, or approximately 4200 mg, or approximately 4550 mg, or approximately 4900 mg, or approximately 5250 mg, or approximately 5600 mg, or approximately 5950 mg, or approximately 6300 mg, or approximately 6650 mg. In another specific embodiment, the anti-alpha-synuclein monoclonal antibody is given according to the invention at a dose of 1050 mg, 2100 mg, or 4200 mg. In one aspect, the antibody directed against alpha-synuclein is given in a liquid pharmaceutical formulation containing a full-length IgG1 anti-alpha-synuclein monoclonal antibody at a concentration of 20-230 mg / ml, such as 25-225 mg / ml, where the aforementioned antibody includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number : 6 ; The formulation also includes a buffering agent, a pharmaceutically acceptable stress-reducing agent, and a pharmaceutically acceptable surfactant. The pH of the formulation is between 4.5 and 7.5, such as between 5.0 and 7.0, or between 5.5 and 6.5, such as 6.0. Other features and advantages of the invention applicable to these aspects and embodiments are made clear from the following detailed description of the invention, the experimental section, and the elements of protection. Brief description For drawings It is clear Figure 1 The expected relationship between doses and exposure in cerebrospinal fluid (CSF) and the percentage of free alpha-synuclein. It is clear Figure 2 Principle of competitive enzyme-linked immunosorbent assay (ELISA). After pre-incubation with increasing concentrations of alpha-synuclein (aSN) monomer or its fibrils, free IgG binds to the laminated aSN monomer and is detected using an antibody directed against human IgG (H+L) labeled with HRP (left). The levels of bound IgG, which are inversely proportional to the concentration of aSN monomer or its fibrils, are plotted as relative fluorescence units, and IC50 values ​​are calculated using a four-parameter nonlinear fitting model (right). It is clear Figure 3 Representative correlation curves of the GM37 Variant 2 with the monomer (R2 = 0.9895) and the fibrillar aSN (R2 = 0.994). It is clear Figure 4 Median (including quartiles) of plasma GM37 Variant 2 concentration (ng / mL) versus time in healthy (A) and patient (B) patients after administration of a single dose of GM37v2 at each dose level. It is clear Figure 5 GM37 Variant 2 plasma concentrations after dose-versus-time (logarithmic scale) standardization at each dose level. It is clear Figure 6 Free plasma alpha-synuclein concentrations versus time in healthy (A) and sick (B) patients after administration of a single dose of GM37v2 at each dose level. It is clear Figure 7 Free / total plasma alpha-synuclein concentrations versus time in healthy (A) and patient (B) treated subjects after administration of a single dose of GM37v2 at each dose level. It is clear Figure 8 Free / total alpha-synuclein plasma concentrations versus plasma concentrations of the GM37 Variant 2 in individuals. It is clear Figure 9 A competitive ELISA assay was used to measure the binding of four antibodies—GM37 wt, GM37 var 1, GM37 var 2, and GM37 var 3—to human alpha-synuclein. Alpha-synuclein-coated plates were used to detect the amount of antibody remaining after pre-incubation of each antibody in a solution (0.3 µg / mL) with increasing concentrations of alpha-synuclein (0–1000 nM). All four antibodies showed similar binding to alpha-synuclein. compare Figure 10 The effect of antibodies directed against alpha-synuclein on phosphorylated alpha-synuclein levels in mouse primary neurons treated with pathological alpha-synuclein fibroblast seeds. Primary neurons were treated with seeds (10 ng) in the presence or absence of four patent-approved antibodies: GM37, GM37 var 1, GM37 var 2, and GM37 var 3 (2 μg). Neurons were fixed and stained after 3 weeks and then analyzed using the Cellomiks ARRAYSCAN™ system to detect positive alpha-synuclein phosphoserine 129 spots. Cells treated with the seeds alone or with the control antibody of isotype B12 showed a marked increase in phosphorylation levels. Cells treated with GM37wt and the three variants were able to inhibit alpha-synuclein phosphorylation, and all exhibited the same phosphorylation level as untreated cells. The data are presented as mean ± standard deviation (SD) calculated from seven images per well in five wells. Number = 2. It is clear Figure 11 Percentage concentrations of free / total alpha-synuclein in cerebrospinal fluid (CSF) in patients with Parkinson's disease (PD) according to the GM37v2 dose on day 3 and day 21 of the study described in Example 3 (number = 15). It is clear Figure 12 The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA was assessed. A 19% clinical slowing of disease progression was observed in MSA patients treated with GM37var2 compared to the placebo group, as evaluated using the UMSARS overall score. It is clear Figure 13 The clinical effect of GM37v2 in the treatment of MSA. A 22% slowing of clinical disease progression was observed in MSA patients treated with GM37var2 compared to the placebo group when assessing the treatment effect using the first part of the UMSARS scale. It is clear Figure 14 The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA was assessed. A 17% clinical slowing of disease progression was observed in MSA patients treated with GM37var2 compared to the placebo group when the treatment effect was assessed using the second part of the UMSARS scale. It is clear Figure 15 The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA was assessed. A 27% slowing of clinical disease progression was observed in MSA patients treated with GM37var2 compared to the placebo group when the treatment effect was assessed using the modified UMSARS scale. It is clear Figures 16a and 16b The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA was investigated. A 50% slowing of clinical disease progression was observed in MSA-C patients treated with GM37var2 compared to the placebo group when assessing the treatment effect using the modified UMSARS scale. It is clear Figures 17 A and 17b The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA. A 42% slowing of clinical disease progression was observed in early MSA patients treated with GM37var2 compared to the placebo group when assessing the effect of treatment using the modified UMSARS scale. It is clear Figures 18a and 18b The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA. Improvement in treatment effects was observed in MSA patients treated with GM37var2 compared to the placebo group when assessing the treatment effect using the fourth part of the UMSARS scale - Total Disability Score or the Overall Clinical Impression Scale - Disease Severity. It explains Figures 19a-19c The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA. Volumetric analysis using MRI showed less local volume reduction in the pons and cerebellar white matter at week 48 in MSA patients treated with GM37var2 compared to the placebo group. It is clear Figure 20 The clinical effect of administering GM37v2 every 4 weeks in the treatment of MSA was observed. A trend toward a greater decrease in the level of nerve fiber light chains in the CSF was noted in MSA patients treated with GM37var2 compared to the placebo group. Definitions The term "full-length antibody" refers to an antibody that is complete in its entirety, or an antibody that is essentially full-length. This term specifically refers to an antibody with heavy chains containing the Fc region. Naturally occurring antibodies are typically tetramers that usually include at least two heavy (H) chains and at least two light (L) chains. Each heavy chain consists of a variable heavy chain domain (abbreviated here as VH) and a fixed heavy chain domain, usually composed of three subdomains (CH1, CH2, and CH3). For example, heavy chains can be selected from the IgG isotype (including the IgG1, IgG2, IgG3, and IgG4 subtypes). Each light chain consists of a variable light chain domain (abbreviated here as VL) and a fixed light chain domain (CL). Light chains include kappa and lambda chains. Both the VH and VL regions can also be divided into highly heterogeneous regions, known as "complement-limiting regions," interspersed with more conserved regions in the sequence, called "frame regions" (FR).Both VH and VL consist of three CDR and four FR regions, arranged from the amino terminus to the carboxyl terminus in the following order: FR1-CDR1-FR2-CDR2-FR3-CDR3-FR4 (or J region). The variant domains in the heavy and light chains contain a binding site that interacts with the antigen. In some formulations, the full-length antibody includes a variant that can be classified as a "product-related substance" according to the International Coordinating Council (ICH) Q6B guidelines. Product-related substances are defined as "molecular variants of the desired product formed during manufacturing and / or storage that retain biological activity and do not have a detrimental effect on the safety or efficacy of the pharmaceutical product. These variants possess properties similar to the desired product and are not considered impurities.""These molecular variants of antibodies intended for use in accordance with the invention are meant to include, for example, N-terminal modifications such as the formation of N-terminal pyroglutamate (pyroGlu), such as cleavage, or incomplete removal of signaling peptides in light or heavy chains, deaminization of asparagine (Asn), isomerization of aspartate (Asp), formation of succinimide, hydrolysis of succinimide, oxidation, cysteine-related modifications such as the presence of free cysteine ​​residues (Cys), or such as the substitution of disulfide bonds (rearrangement), or such as the formation of trisulfide bonds, or such as the formation of thioether bonds, or such as the racemic transformation of cysteine, glucosization, and glycoligandization, and C-terminal modifications such as the removal of Lys from the C-terminus, or such as the removal of both Lys and Gly from the C-terminus, or such as the addition of amide to the C-terminus." The term "epithelium" refers to an antigen-specific molecule capable of binding specifically to an antibody. Epithelis typically consist of surface groups of molecules such as amino acids or sugar side chains, and usually possess specific three-dimensional structural properties, as well as characteristic charge properties. Combinational epithelis are distinguished from linear epithelis in that binding to the former, but not the latter, is always lost in the presence of denaturing solvents. An epithelium may contain amino acid residues that directly participate in binding and other amino acid residues that do not, such as amino acid residues that are effectively blocked by the specific antigen-binding peptide (in other words, the amino acid residue lies within the signature occupied by the specific antigen-binding peptide).The term “112-117 epitope” or “112-117 amino acid epitope” refers to a region of human alpha-synuclein that contains at least 4 of the 6 amino acid residues located at positions 112-117 of human alpha-synuclein, as well as all of the 6 amino acid residues located at positions 112-117 of human alpha-synuclein, provided that the epitope does not contain any residues from positions 1-111 (including any residues from positions 106-111) of human alpha-synuclein, nor any residues from positions 118-140 (including residues from positions 118-120) of human alpha-synuclein.As used here, the antibody intended for use according to the invention that is said to bind to an epitope located within amino acids 112-117 is capable of specific binding to human alpha-synuclein by binding to at least 4 residues of the 6 amino acids constituting epitope 112-117, such as binding to the 6 amino acids constituting epitope 112-117, without binding to any residues from positions 1-111 (including any residues from positions 106-111) of human alpha-synuclein, nor any residues from positions 118-140 (including residues 118-120) of human alpha-synuclein. The term "human antibody" (which may be abbreviated to "humAb" or "HuMab"), as used here, means antibodies containing both variable and fixed domains derived from human germline immunoglobulin sequences. Human antibodies intended for use under the invention may include amino acid residues not encoded by human germline immunoglobulin sequences (for example, mutations introduced by random or site-directed mutations in vitro, during gene rearrangements, or by somatic mutation in vivo). The term “humanized” refers to a molecule, generally prepared using recombinant DNA techniques, that contains an antigen-binding site derived from a non-human immunoglobulin, while the rest of the immunoglobulin structure is based on the structure and / or sequence of a human immunoglobulin. The antigen-binding site may consist of either the complete variable domains of a non-human antibody fused to human constant domains, or only the complementation-specific regions (CDRs) of those variable domains after grafting onto suitable human frame regions within human variable domains. The frame residues of these humanized molecules may be wild-type (e.g., entirely human) or may be modified to contain one or more amino acid substitutions not present in the human antibody whose sequence was used as the basis for the humanization process. Another approach focuses not only on providing constant domains derived from human sources but also on modifying the variable domains to reconfigure them as closely as possible to the human type.It is known that the variable domains of both heavy and light chains contain three complementation-specific regions (CDRs) that vary according to the antigens involved and determine the ability to bind, surrounded by four frame regions (FRs) that are relatively conserved within the species and are thought to provide a scaffold for the CDR regions. When non-human antibodies directed against a specific antigen are prepared, the variable domains can be "reconstructed" or "humanized" by grafting the CDR regions derived from the non-human antibody onto the FR regions of the human antibody to be modified. In the present context, the term “treatment” or “cure” means the therapeutic intervention and clinical care provided to a patient for the purpose of alleviating, reducing, completely or partially stopping, eliminating, delaying, or slowing the progression of one or more clinical manifestations of a disease. For the purposes of this invention, the terms “treatment” or “cure” also refer to any approach aimed at achieving a beneficial or desirable clinical outcome. Such “beneficial or desirable clinical outcomes” include, but are not limited to, symptom relief, reduction of the extent of the disorder or illness, stabilization of the condition or disorder (i.e., preventing its worsening), delaying or slowing the progression of the disease or disorder, improvement or relief of the disease or disorder, or inducing partial or complete remission of the disease or disorder. In a particular embodiment, the "treatment" or "therapeutic effect" is to delay or slow disease progression in a patient with a synopathy, and in a particular embodiment, this synopathy is MSA. This MSA can be selected from one or more subtypes of MSA, such as clinically confirmed MSA, clinically probable MSA, possible MSA, or likely MSA.MSA type C or MSA type P. In another sense, "cure" means delaying disease onset in a patient with prodromal synopathy. Treatment can be assessed by quantifying clinical efficacy or therapeutic effect by measuring the degree of slowing or delay in disease progression, based on longitudinal changes compared to baseline on the Unified Multiple Systemic Atrophy Rating Scale (UMSARS) within the total score of parts one and two (UMSARS TS), within the first part of the modified UMSARS scale (mUMSARS), or on the abbreviated UMSARS scale (aUMSARS) until the end of treatment (EoT), i.e., at the end of a treatment period of 24 weeks, 48 ​​weeks, 72 weeks, 96 weeks, or longer. Treatment can also be assessed by quantifying clinical efficacy or therapeutic effect through evaluating the slowing or delay in disease progression, based on longitudinal changes compared to baseline within the scores of UMSARS Part 1, the modified UMSARS Part 1 (mUMSARS), and / or UMSARS Part 2 up to the end of EoT treatment. This disease progression can also be assessed by the magnitude of the change from baseline.End-of-treatment EoT is assessed in UMSARS TS scores, and / or UMSARS Part 1, and / or mUMSARS and / or UMSARS Part 2 scores. Disease progression can also be assessed by longitudinal changes compared to baseline in the abbreviated UMSARS (aUMSARS) scale up to the end of EoT, or by changes in brain volume, using volumetric magnetic resonance imaging (vMRI), or by changes in blood concentrations of neuronal filament light chains (NfL). Treatment can also be assessed by quantifying clinical efficacy or therapeutic effect by measuring the slowing or delay in disease progression, as measured by longitudinal changes compared to baseline in one or more of the following indicators: Schwab and England Activity of Daily Living (SE-ADL) score; or change compared to baseline in the Clinical General Impression-Severity (CGI-S) score; or change compared to baseline in the Patient General Impression-Severity (PGI-S) score; or change compared to baseline in the Assessor General Impression-Severity (OGI-S) score. Or the change compared to baseline in the score on the system symptom change scale.The specific composite neurological change (COMPASS Select Change); or the change compared to baseline in the UMSARS Part 4 score; or the change compared to baseline in the speech, swallowing, falling, and walking items, as assessed using the UMSARS Part 1 item scores; or the change compared to baseline in the rate, causes, and consequences of falls, as assessed using fall logs or diaries; or the change compared to baseline in the EuroQol 5D-5L score; or the change compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI); or the change compared to baseline in tissue integrity, as measured using diffusion tensor magnetic resonance imaging (DTI); or the change compared to baseline in blood NfL light chain concentrations; or the change compared to baseline in heart rate, blood pressure, and postural symptoms, as assessed in the UMSARS Part 3. Or the change compared to baseline in gait parameters or fall rate, as measured by digital sensors.For wearable devices capable of tracking relevant gait parameters and / or recording falls; or changes compared to baseline in cerebral blood flow, as measured by magnetic resonance imaging using arterial spindle labeling (ASL); or changes compared to baseline in total tau protein and NfL chain concentrations in cerebrospinal fluid (CSF); or changes compared to baseline in pathological alpha-synuclein species in CSF. The patient to be treated or diagnosed can be identified by any method or diagnostic standard recognized in the relevant field. The term "kd" refers to (second -1 Or 1 / second), as used here, is the dissociation rate constant for the reaction between the antibody and the antigen. This value is also denoted by the symbol koff. The term "ka" (mol) refers to -1 x seconds -1 Or 1 / mol.sec), as used here, the constant of the binding rate between the antibody and the antigen. The term "KD" (molar), as used here, refers to the dissociation equilibrium constant for the reaction between the antibody and the antigen, and is calculated by dividing the value of kd by the value of ka. The value of KD can be determined by methods such as those described in Example 6A, or by other methods known in the field. The term "KA" (mol) refers to -1 Or 1 / mol), as used here, the binding equilibrium constant between the antibody and the antigen, calculated by dividing the ka value by the kd value. The term "IC50," as used here, refers to the concentration of the antibody that achieves 50% of its maximum inhibitory effect. The precise value of IC50, usually expressed in nanomolar units, depends on the type of assay used and therefore cannot be directly compared between different assays. The term "Emax," as used here, refers to the maximum effect achieved by the antibody at high concentrations, i.e., when all alpha-synuclein molecules are bound to the antibody. The term "affinity," as used here, refers to the overall strength of the antibody-antigen complex. In this context, it denotes the sum of individual non-covalent binding interactions between an IgG molecule and its antigen. The term “Cmax,” as used here, refers to the highest concentration of the antibody reached in the plasma of the patient after the said antibody has been administered intravenously. The term "tmax," as used here, refers to the time required to reach the Cmax value after antibody infusion. The term "use in accordance with the invention," as used in this disclosure, encompasses all described uses and methods, including the use of the antibody in the treatment of synovial disorders or prodromal synovial disorders, methods of treating such disorders, and the use of the anti-alpha-synoclane monoclonal antibody in the manufacture of a drug for the treatment of synovial disorders or prodromal synovial disorders. This use may include administering an anti-alpha-synoclane monoclonal antibody, such as GM37v2, to a patient in need using appropriate doses, appropriate dosing schedules, and / or in a suitable pharmaceutical formulation. This invention also provides for the pharmaceutical formulations or formulations described herein. The terms "pharmaceutical formulation" and "formulation" are used interchangeably in this application. The term "stable formulations" refers to a formulation that can be stored for a specified period, in this application, 6 months or more, under specific storage conditions. These conditions are the usual storage conditions for antibody formulations, such as storage at approximately 5°C, so that the protein in the formulation retains largely its physical, chemical, and / or biological stability. Several analytical techniques for measuring protein stability are well-established in the field, and some of these techniques are also described in the experimental section here. Stability can be assessed at a specific temperature and over a specific period. In certain formulations, the pharmaceutical formulation is stable at approximately 40°C for at least 1, 2, 3, 4, 5, 6, 7, 14, 21, or 28 days, or longer. In certain formulations, the pharmaceutical formulation is stable at approximately 40°C ± 3°C for a period of not less than approximately 1, 2, 3, 4, 5, 6, 7, or 8 weeks or more.In certain formulations, the pharmaceutical formulation is stable at approximately 25°C for a period of not less than 1, 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 more. In certain formulations, the pharmaceutical formulation is stable at approximately 5°C ± 3°C for a period of not less than 1, 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 more. In certain embodiments, the pharmaceutical formulation is stable at approximately -20°C ± 3°C for a period of not less than 1, or 2, or 3, or 4, or 5, or 6, or 7, or 8, or 9, or 10, or 11, or 12, or 13, or 14, or 15, or 16, or 17, or 18, or 19, or 20, or 21, or 22, or 23, or 24, or 25, or 26, or 27, or 28, or 29, or 30, or 31, or 32, or 33, or 34, or 35, or 36, or 37, or 38, or 39, or 40, or 41, or 42, or 43, or 44, or 45. Or 46, or 47, or 48 months or more.In addition, it is preferable that the pharmaceutical formulation maintains its stability after freezing (at, for example, -20°C, -40°C, or -70°C) and then thawing, for example, after 1, 2, 3, 4, or 5 freeze-thaw cycles. Stability can be assessed qualitatively and / or quantitatively using a variety of methods, including the assessment of protein aggregate formation (for example, by volumetric exclusion chromatography, and / or by turbidity measurement, and / or by visual inspection); by assessing charge heterogeneity using cation exchange chromatography, isoelectric capillary focusing (icIEF), or banded capillary electrophoresis; amino-terminal or carboxyl-terminal sequencing analysis; mass spectrometry analysis; SDS-PAGE analysis to compare the antibody in its reduced and non-reduced states; or peptide mapping analysis (for example, tryptic or LYS-C analysis). Or assess the biological activity of the antibody or its ability to bind to the antigen; or other known methods.Instability may include one or more of the following manifestations: aggregation, deaminosis (e.g., deaminosis of Asn), oxidation (e.g., oxidation of Met), isomerization (e.g., isomerization of Asp), cleavage / hydrolysis / fragmentation (e.g., fragmentation of the hinge region), succinimide formation, presence of unbound cysteine(s), N-terminal elongation, C-terminal processing, glucosity variations, or others. The term “low viscosity formulation” means a liquid pharmaceutical formulation whose viscosity is less than approximately 20 centipoes, or less than 15 centipoes, or less than 14 centipoes, or less than 13 centipoes, or less than 12 centipoes, or less than 11 centipoes, or less than 10 centipoes, or less than 9 centipoes, or less than 8 centipoes, or less than 7 centipoes, or less than 6 centipoes, or less than 5 centipoes. In this application, the term "buffering agent" means a buffer solution that resists changes in pH by virtue of the presence of a conjugated acid-base pair. Ideally, the buffering agent or agents in this invention (the terms are used here interchangeably) should maintain the pH of the formulation within a range of approximately 4.5 to approximately 7.5, such as approximately 5.5 to approximately 6.5, for example, between 5.7 and 6.4, or between 5.8 and 6.3, or between 5.9 and 6.2. In one embodiment, the pH of the buffering agent is 5.5, 5.6, 5.7, 5.8, 5.9, 6.0, 6.1, 6.2, 6.3, 6.4, 6.5, or 7.0. Histidine buffers (such as L-histidine) are an example of suitable buffering agents for adjusting pH within this range. Other examples of buffering agents include acetate, citrate, tartrate, histidine (such as L-histidine), glutamate, phosphates, tris, glycine, bicarbonate, succinate, sulfate, nitrate, and any combination thereof. In some formulations, the buffering agent is chosen from sodium phosphate, histidine (such as L-histidine), citric acid, sodium citrate, sodium acetate, or any combination thereof.In one specific embodiment, the buffering agent is a histidine buffer (such as L-histidine) or a mixture of histidine buffers.In this present application, the term "surfactant" means a surface-active agent, preferably a non-ionic surfactant. Examples of surfactants here include polysorbates (e.g., polysorbate 20, polysorbate 80); poloxamer (e.g., poloxamer 188); Triton; Triton X-100; sodium dodecyl sulfate (SDS); sodium lauryl sulfate; sodium octyl glycoside; lauryl-, myristyl-, linoleyl-, or stearyl-sulfobetaine compounds; lauryl-, myristyl-, linoleyl-, or stearyl-sarcosine compounds; and linoleyl-, myristyl-, or cetyl-betaine compounds. Loramidopropyl-, cocamidopropyl-, linoleimidopropyl-, myristamidopropyl-, palmidopropyl-, or isostearamidopropyl-betane compounds (e.g., loramidopropyl); myristamidopropyl-, palmidopropyl-, or isostearamidopropyl dimethylamine compounds; sodium methylcocoyl, or disodium methyloleate taurate; as well as polyethylene glycol, polypropylene glycol, and ethylene glycol and propylene glycol copolymers.In one specific embodiment, the pharmaceutically acceptable surfactant is polysorbate 80, also known as Tween 80. In this application, the term "tensioning agent" refers to an excipient capable of imparting isotonic properties to a liquid pharmaceutical formulation. Isotonic means that the formulation has, to a large extent, the same osmotic pressure as human blood plasma. The osmotic pressure of isotonic formulations is typically between approximately 250 and 350 mS / mol. Examples of tensioning agents include mannitol, sorbitol, lactose, dextrose, trehalose, sodium chloride, potassium chloride, glycerol, and glycerol. In one specific embodiment, a tensioning agent is a suitable salt such as sodium chloride (NaCl). In this context, the term "bulking agent" refers to an excipient that provides additional stability to a liquid pharmaceutical formulation. Examples of bulking agents include the following major classes of excipients: sugars and polyols (such as sucrose, trehalose, glucose, lactose, sorbitol, mannitol, and glycerol); amino acids (such as arginine, aspartic acid, glutamic acid, lysine, glycine, glutamate, histidine, methionine, or alanine); and polymers and proteins (such as gelatin, PVP, PLGA, PEG, dextran, cyclodextrin and its derivatives, starch derivatives, and HSA or BSA). In one specific embodiment, the bulking agent is sucrose. The term "histidine buffer" or "histidine" refers to histidine buffering agents or any mixture thereof, such as histidine, L-histidine, L-histidine hydrochloride, L-histidine monohydrochloride, L-histidine monohydrate, L-histidine hydrochloride monohydrate, or any mixture thereof. In one specific formulation, a histidine buffer is a mixture of L-histidine and L-histidine monohydrochloride. The term “towards”, as used here, means ±10% of the specified value. Detailed description of the invention This invention relates to the appropriate clinical uses of monoclonal antibodies directed against human alpha-synuclein for use in the treatment of synonucleopathies or prodromal synonucleopathies. The inventors of this invention developed a method for treating MSA in humans using antibodies targeting alpha-synuclein. The data in the experimental section (Example 8 and Figures 12-20) showed a consistent trend indicating the ability of the specific anti-alpha-synuclein antibody, GM37var2 (Amlenetug), to slow clinical disease progression in treated patients with MSA. The results also showed a slowing of both functional and motor deterioration in treated patients with early-stage MSA who received GM37var2 (Amlenetug), as measured by the overall and sub-scores of the UMSARS scale. This slowing was 27% when using the mUMSARS scale to assess the treatment effect. In addition, subgroup analysis showed that the therapeutic effects were more pronounced in MSA patients diagnosed with MSA-C and / or early MSA, as evidenced by a lower overall UMSARS score at baseline, for example, when the UMSARS baseline TS value was less than 40. Furthermore, the observed trends in other clinically relevant efficacy indicators related to disease severity and patient function supported the therapeutic effects assessed using UMSARS measures. Volumetric analysis using magnetic resonance imaging of the pons and cerebellum white matter showed a slowing of white matter volume loss in the GM37var2 (Amlenetug) treatment group. The data presented here, taken together, indicate a clinical benefit to treating MSA patients with GM37var2 (Amlenetug), and notably the therapeutic effect was most pronounced in MSA patients with early MSA and / or those diagnosed with MSA-C. In one respect, the invention provides a monoclonal antibody directed against alpha-synuclein for use in the treatment of synopathies or prodromal synopathies, the said use of which involves the intravenous administration of the said antibody to a person under treatment who has or is at risk of developing a synopathy, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The said monoclonal antibody directed against alpha-synuclein is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence Identification Number: 9 (ILEDMP)) of human alpha-synuclein (Sequence Identification Number: 10). In one aspect, the invention provides a monoclonal antibody directed against alpha-synuclein for use in the treatment of MSA, where the said use involves giving the said antibody to a person undergoing treatment who is suffering from MSA. In one respect, the invention provides a monoclonal antibody directed against alpha-synuclein for use in the treatment of MSA, whereby the said use involves the intravenous administration of the said antibody to a person undergoing treatment who has or is at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The said monoclonal antibody directed against alpha-synuclein is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). On the other hand, the invention provides a method for treating synonucleopathies or prodromal synonucleopathies. The method involves administering a monoclonal antibody directed against alpha-synuclein intravenously to a person undergoing treatment who needs it, such that the person undergoing treatment is suffering from or at risk of developing a synonucleopathy, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The monoclonal antibody directed against alpha-synuclein said is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). On the other hand, the invention provides a method for treating MSA. The method involves giving a monoclonal antibody directed against alpha-synuclein to a person undergoing treatment who needs it, as the person undergoing treatment is suffering from MSA. On the other hand, the invention provides a method for treating MSA. The method involves administering a monoclonal antibody directed against alpha-synuclein intravenously to a person undergoing treatment who needs it, where the person undergoing treatment is infected with MSA or at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The monoclonal antibody directed against alpha-synuclein is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). On another side, the invention also provides for the use of a monoclonal antibody directed against alpha-synuclein in the manufacture of a drug for the treatment of synonucleopathies or prodromal synonucleopathies, where the aforementioned use involves the intravenous administration of the aforementioned antibody to a person under treatment who has or is at risk of developing a synonucleopathy, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The aforementioned monoclonal antibody directed against alpha-synuclein is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence Identification Number: 9 (ILEDMP)) of human alpha-synuclein (Sequence Identification Number: 10). On another front as well, the invention provides for the use of a monoclonal antibody directed against alpha-synuclein in the manufacture of a drug to treat MSA, where the aforementioned use involves giving the aforementioned anti-alpha-synuclein antibody to a person undergoing treatment who suffers from MSA. On another side, the invention also provides for the use of a monoclonal antibody directed against alpha-synuclein in the manufacture of a drug for the treatment of MSA, where the aforementioned use involves the intravenous administration of the aforementioned antibody to a person undergoing treatment who has MSA or is at risk of developing MSA, at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, or between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. The aforementioned monoclonal antibody directed against alpha-synuclein is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). In certain embodiments, the monoclonal antibody directed against alpha-synuclein has an estimated KD value for binding to the oligomeric form of alpha-synuclein of approximately 0.1-1.0 nanomolar, such as 0.2-0.8 nanomolar, 0.4-0.6 nanomolar, or approximately 0.5 nanomolar. In certain formulations, the monoclonal antibody directed against alpha-synuclein has a KD value of approximately 30–40 nM for the monomeric form of alpha-synuclein, such as 32–38 nM, 34–37 nM, or approximately 36 nM, and an estimated KD value of approximately 0.1–1.0 nM for the oligomeric form of alpha-synuclein, such as 0.2–0.8 nM, 0.4–0.6 nM, or approximately 0.5 nM. In one formulation, the oligomeric-to-monomeric binding ratio is enhanced by approximately 60–70-fold, such as 62–68-fold, 64–66-fold, or 65-fold. This enhancement in binding between the two forms is explained in more detail in the experimental section and is referred to as "desire enhancement." This enhanced binding between the two isoforms is referred to as "enhancing desirability" in this finding. In certain isoforms, the monoclonal antibody directed against alpha-synuclein has a human half-life of approximately 25–35 days, such as approximately 4 weeks, or approximately 27–33 days, or approximately 28 days, or approximately 28–32 days, or approximately 30 days, or approximately 28–30 days. In one embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number :2 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number :3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number :4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number :5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes a heavy chain consisting of a variable domain. Number Definition of sequence :7 A light series consisting of a variable range Serial ID number :8 . In one embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number :33 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number :3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number :4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number :5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes a heavy chain consisting of a variable domain. Serial ID number :30 A light series consisting of a variable range Serial ID number :8 . In one embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes a variable band of heavy chain Serial ID number :31 and a variable range for a light chain Serial ID number :8 . In one embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 35 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes a heavy chain consisting of a variable domain. Serial ID number :32 A light series consisting of a variable range Serial ID number :8 . In a specific embodiment, the monoclonal antibody directed against alpha-synuclein intended for use under the invention is a full-length human antibody. In such an embodiment, the monoclonal antibody directed against alpha-synuclein could be, for example, a human IgG1 antibody. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use in accordance with the invention includes a fixed area for a human IgG1 heavy chain and / or a fixed area for a human kappa light chain. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention includes a fixed band of heavy chain as defined in Serial ID number :18 and / or a fixed range for a kappa-type light chain as defined in Serial ID number :17 . In one particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use under the invention is the GM37 antibody, or one of its variants: GM37 Variant 1, GM37 Variant 2, or GM37 Variant 3. In a preferred embodiment, the antibody is GM37v2 (Amlenetug). In another preferred embodiment, the antibody is Amlenetug. In one formulation, the alpha-synuclein monoclonal antibody intended for use according to the invention is administered at a dose greater than 700 mg and less than 7000 mg, such as a dose between 900 mg and 5000 mg, between 1000 mg and 4500 mg, or between 2000 mg and 4300 mg. In a specific formulation, the alpha-synuclein monoclonal antibody is administered at 3- to 5-week intervals, or the antibody is administered to the patient according to another dosing regimen that substantially provides the same area under the curve (AUC) for exposure to the antibody, or substantially provides the same estimated binding to the alpha-synuclein oligomeric target in the patient's cerebrospinal fluid (CSF). In some formulations, the monoclonal antibody directed against alpha-synuclein, as prescribed for the invention, is administered every 6 weeks, every 5 weeks, every 4 weeks, every 3 weeks, every 2 weeks, or every week. In other formulations, the monoclonal antibody directed against alpha-synuclein, as prescribed for the invention, is administered every 20 days, every 21 days, every 22 days, every 23 days, every 24 days, every 25 days, every 26 days, every 27 days, every 28 days, every 29 days, every 30 days, every 31 days, every 32 days, every 33 days, every 34 days, every 35 days, every 36 days, every 37 days, every 38 days, every 39 days, or every 40 days. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given every 3-5 weeks, such as every 4 weeks or once a month, such as every 25-31 days, such as every 28-30 days. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose of approximately 75 mg, or approximately 225 mg, or approximately 750 mg, or approximately 2250 mg, or approximately 4500 mg, or approximately 9000 mg. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose between 4000 mg and 7000 mg, such as a dose between 4000 mg and 6500 mg, or between 4200 mg and 6300 mg, such as 4200 mg or 6300 mg. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose of approximately 750 mg, or approximately 1050 mg, or approximately 1400 mg, or approximately 1750 mg, or approximately 2100 mg, or approximately 2450 mg, or approximately 2800 mg, or approximately 3150 mg, or approximately 3500 mg, or approximately 3850 mg, or approximately 4200 mg, or approximately 4550 mg, or approximately 4900 mg, or approximately 5250 mg, or approximately 5600 mg, or approximately 5950 mg, or approximately 6300 mg, or approximately 6650 mg. In one additional specific embodiment, the monoclonal antibody directed against alpha-synuclein, intended for use according to the invention, is given at a dose of approximately 1050 mg, or approximately 2100 mg, or approximately 4200 mg, or approximately 6300 mg. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is given at the dose specified above by intravenous infusion over a period of 30 minutes ±10 minutes, such as 20 minutes, 25 minutes, 30 minutes, 35 minutes, or 40 minutes. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is given at the dose specified above by intravenous infusion over a period of 15 minutes ± 5 minutes, e.g., 10 minutes, 15 minutes, or 20 minutes. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at the dose specified above by intravenous infusion at a rate of approximately 30 mg / min to approximately 150 mg / min, such as approximately 35 mg / min, or approximately 70 mg / min, or approximately 140 mg / min. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at the dose specified above by intravenous infusion at a rate of approximately 25 mg / min to approximately 300 mg / min, such as 60 mg / min to approximately 300 mg / min, such as approximately 70 mg / min, or approximately 140 mg / min, or approximately 280 mg / min. In one embodiment, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is given in a quantity and frequency sufficient to achieve an estimated steady-state mean concentration of the said antibody in the cerebrospinal fluid (CSF) of not less than 0.5 nanomolar, such as not less than 1 nanomolar, 2 nanomolar, 3 nanomolar, 4 nanomolar, 5 nanomolar, 6 nanomolar, 7 nanomolar, 8 nanomolar, 9 nanomolar, 10 nanomolar, 11 nanomolar, 12 nanomolar, 13 nanomolar, 14 nanomolar, or 15 nanomolar. On the other hand, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is given in a quantity and frequency sufficient to achieve an estimated binding to the target for alpha-synuclein oligomeric forms in cerebrospinal fluid (CSF) of not less than 50%, such as not less than 55%, 60%, 75%, 77%, 80%, 82%, 85%, 87%, 90%, 92%, 95%, 97%, or 99%. In another formulation, the monoclonal antibody directed against alpha-synuclein, formulated according to the patent, is intended for use in the treatment of synonucleopathies. These synonucleopathies may be selected from a group that includes: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, autonomic nervous system failure, and multiple system atrophy (MSA). The treatment may aim to slow or delay the progression of the synonucleopathy (e.g., the progression of MSA) or delay the onset of the disease if the patient has a precursor synonucleopathy. In a particular incarnation, the synovial disorder to be treated is Parkinson's disease (PD). On another side as well, the synovial disorder that needs to be treated is Lewy body dementia (DLB). On another side, the synocular disorder to be treated is multiple system atrophy (MSA). In such a manifestation, the person undergoing treatment with MSA has either the parkinsonian-type MSA-P or cerebellar-type MSA-C subtype, or has been diagnosed with clinically possible or probable MSA, and this possible or probable MSA can also be of the parkinsonian-type MSA-P or cerebellar-type MSA-C subtype, or has been diagnosed with clinically confirmed or clinically probable MSA, and this can also be of the parkinsonian-type MSA-P or cerebellar-type MSA-C subtype. In another embodiment, the diagnosis of MSA is based on the presence of one or more appropriate MSA biomarkers identified in a patient undergoing the aforementioned treatment. These biomarkers can be selected from a range that includes: physiological biomarkers, biological biomarkers, genetic biomarkers, molecular biomarkers, histological biomarkers, radiological biomarkers, imaging biomarkers, behavioral biomarkers, or digital biomarkers. In a similar further embodiment, a patient undergoing treatment with MSA, or who has been clinically diagnosed with probable or likely MSA or other MSA subtypes, can be identified using established clinical assessment methods and / or diagnostic techniques recognized in the field.In another similar embodiment, a person undergoing treatment who has multiple systemic atrophy (MSA) or who has been diagnosed with probable or clinically likely MSA or other MSA subtypes can be identified by the appearance of motor and / or autonomic nervous system (erectile or urinary) symptoms of MSA within the last 5 years, such as the last 4 years, 3 years, 2 years, within the last year, or within the last 6 months. In another similar embodiment, a person undergoing treatment with multiple systemic atrophy (MSA), or who has been clinically diagnosed with probable or likely MSA or other MSA subtypes, can be identified by a score ≤ 16 on Part 1 of the UMSARS scale (excluding item 11 related to sexual function). In yet another similar embodiment, a person undergoing treatment with MSA, or who has been clinically diagnosed with probable or likely MSA or other MSA subtypes, can be identified by a score ≥ 22 on cognitive performance using the Montreal Cognitive Assessment (MoCA). In another similar incarnation, the patient undergoing treatment for multiple systemic atrophy (MSA) has MSA-C. In another similar incarnation, the patient undergoing treatment for MSA has MSA-P. In another similar incarnation, the patient undergoing treatment for MSA has clinically possible or probable MSA-C. In another similar incarnation, the patient undergoing treatment for MSA has clinically possible or probable MSA-P. In another similar incarnation, the patient undergoing treatment for MSA has clinically confirmed or probable MSA. In another similar incarnation, the patient undergoing treatment for MSA has clinically confirmed or probable MSA. In another similar incarnation, the patient undergoing treatment for MSA has clinically confirmed or probable MSA-C. In another similar scenario, a person undergoing treatment for multiple systemic atrophy (MSA) has early-stage MSA. In another similar embodiment, the person undergoing treatment who has multiple systemic atrophy (MSA) has MSA at a stage of the disease in which the disease has not yet caused significant deterioration in the said patient, such as having an overall UMSARS TS score of less than 40 (for example, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, 20-25, 10-20, 15-20, or 10-15). In another similar incarnation, the person undergoing treatment who suffers from multiple systemic atrophy (MSA) has early-onset MSA.In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein. In another similar embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein. In another embodiment, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is intended for use in the treatment of prodromal synonucleopathies in a person undergoing treatment who is at risk of developing a synonucleopathy. The person undergoing treatment can be identified by the demonstration of one or more clinical indicators of prodromal synonucleopathies selected from a group that includes: REM rapid eye movement (RBD) sleep behavior disorder such as isolated RBD (iRBD), olfactory disorder such as hyposmia, abnormal cognitive performance on neuropsychological tests, mild motor dysfunction or abnormal motor performance assessed by objective tests, color vision disorder, autonomic nervous system disorders (such as constipation, urinary symptoms, erectile dysfunction, and orthostatic hypotension), reduced black striatal dopaminergic binding in the pituitary and striatum (abnormal DAT-SPECT), and a genotype associated with an increased risk of phenotypic transformation such as mutations in the glucocerebrosidase enzyme (encoded by the GBA gene).In such a scenario, a patient undergoing treatment at risk of developing synonucleosis can be identified by exhibiting an RBD disturbance such as isolated RBD (iRBD) and at least one additional clinical sign of prodromal synonucleosis, such as anosmia and / or an abnormal DAT-SPECT. In another similar scenario, a patient undergoing treatment at risk of developing synonucleosis can also be identified by exhibiting an RBD disturbance such as isolated RBD (iRBD), anosmia, and an abnormal DAT-SPECT. In one respect, the pharmaceutical formulation of the monoclonal antibody directed against alpha-synuclein, such as GM37v2, is formulated in one of the specified liquid pharmaceutical formulations as listed in this application. On the other hand, a kit is provided that includes a monoclonal antibody directed against alpha-synuclein intended for use in accordance with the invention. In another embodiment as well, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is expressed in CHO cells or obtained by expressing it in these cells. In one respect, the monoclonal antibody directed against alpha-synuclein, prepared for use according to the invention, is intended for use in the treatment of abnormal alpha-synuclein aggregation in a patient undergoing treatment, in which abnormal alpha-synuclein aggregation has been established in the central nervous system (CNS) of the said patient. In some formulations, treatment with the patented monoclonal antibody targeting alpha-synuclein may continue for weeks, months, a year, or even several years. In other formulations, treatment may be part of a combination therapy, in which the patented monoclonal antibody is given in combination with one or more additional pharmaceutical agents or as adjunctive therapy. These additional pharmaceutical agents may be part of the standard of care used to treat the specific synonucleopathy. For example, in the case of multiple systemic atrophy (MSA), the standard of care may include one or more of the following: drugs intended to relieve Parkinson's-like signs and symptoms, such as levodopa and / or carbidopa, or drugs known to be beneficial in treating autonomic nervous system symptoms (such as urinary symptoms or neurogenic orthostatic hypotension), such as pyridostigmine, midodrine, or droxydopa. Specific doses and dosing regimens Doses and dosing regimens may be expressed as fixed doses, such as a specific amount in mg of the monoclonal antibody intended for use in accordance with the invention (i.e., regardless of the body weight of the person being treated). These doses are described in various embodiments and aspects of this invention, including Table 1 below. In some embodiments, doses or dosing regimens may also be expressed in mg / kg (i.e., doses that vary according to the body weight of the person being treated). Converting fixed doses to doses administered according to body weight (i.e., mg / kg) and vice versa is within the normal skills of a qualified physician. The result of this conversion depends on the body weight of the person being treated with the doses or dosing regimens. In one formulation, the monoclonal antibody directed against alpha-synuclein, formulated for use according to the invention, is administered at a dose of 1000 mg to 4500 mg at 3- to 5-week intervals. Alternatively, the antibody may be administered to the patient according to a different dosing regimen that provides roughly the same estimated binding to the target of alpha-synuclein oligomers in the patient's cerebrospinal fluid (CSF). In another formulation, the antibody is administered to the patient according to a dosing regimen that provides roughly the same estimated binding to the target of alpha-synuclein oligomers in the patient's CSF as a 4200 mg dose of GM37v2 administered approximately every 4 weeks. In some formulations, the monoclonal antibody directed against alpha-synuclein, as prescribed by the invention, is administered every 4 weeks. In other formulations, it is administered monthly. And in yet other formulations, it is administered every 27, 28, 29, 30, or 31 days. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given every 3-5 weeks, such as every 4 weeks or once a month, such as every 28-30 days. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose between 1000 mg and 4500 mg, such as a dose between 2000 mg and 4500 mg, or between 3500 mg and 4500 mg, such as 4200 mg. In one specific formulation, the monoclonal antibody directed against alpha-synuclein, as formulated in the invention, is administered at a dose of approximately 1050 mg, 1400 mg, 1750 mg, 2100 mg, 2450 mg, 2800 mg, 3150 mg, 3500 mg, 3850 mg, or 4200 mg. In another specific formulation, the monoclonal antibody directed against alpha-synuclein, as formulated in the invention, is administered at a dose of 1050 mg, 2100 mg, or 4200 mg. In one embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose of 13 mg / kg to 71 mg / kg, or 14 mg / kg to 64 mg / kg, or 15 mg / kg to 60 mg / kg, or 15 mg / kg, or 30 mg / kg, or 60 mg / kg at 3-5 week intervals, or the said antibody is given to the person being treated according to another dosing regimen that largely provides the same estimated binding to the target of alpha-synuclein oligomer in the patient’s cerebrospinal fluid (CSF). In a particular embodiment, the aforementioned antibody is given to the person undergoing treatment according to a dosing regimen that largely provides the same estimated binding to the target of alpha-synuclein oligomer in the patient’s cerebrospinal fluid (CSF) as would be provided by a 60 mg / kg dose of GM37v2 given approximately every 4 weeks. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose of approximately 1 mg / kg, or approximately 3 mg / kg, or approximately 11 mg / kg, or approximately 32 mg / kg, or approximately 64 mg / kg, or approximately 129 mg / kg. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose between 14 mg / kg and 64 mg / kg, such as a dose between 15 mg / kg and 60 mg / kg, or between 30 mg / kg and 60 mg / kg, such as 60 mg / kg. In a particular embodiment, the monoclonal antibody directed against alpha-synuclein intended for use according to the invention is given at a dose of approximately 11 mg / kg, or approximately 15 mg / kg, or approximately 20 mg / kg, or approximately 25 mg / kg, or approximately 30 mg / kg, or approximately 35 mg / kg, or approximately 40 mg / kg, or approximately 45 mg / kg, or approximately 50 mg / kg, or approximately 55 mg / kg, or approximately 60 mg / kg, or approximately 65 mg / kg, or approximately 70 mg / kg, or approximately 75 mg / kg, or approximately 80 mg / kg, or approximately 85 mg / kg, or approximately 90 mg / kg, or approximately 95 mg / kg. In one additional specific embodiment, the monoclonal antibody directed against alpha-synuclein, intended for use according to the invention, is given at a dose of 15 mg / kg, 30 mg / kg, or 60 mg / kg. In a specific embodiment, the body weight of the patient to be treated ranges between 50 and 110 kg, such as 50 kg, 55 kg, 60 kg, 65 kg, 70 kg, 75 kg, 80 kg, 85 kg, 90 kg, 95 kg, 100 kg, 105 kg, or 110 kg. In the clinical study described in Example 3, the average body weight of the human subjects included in the study was approximately 70 kg. In some embodiments, dosing and dosing regimens according to this invention may also be expressed in terms of the quantity and frequency of administration of a monoclonal antibody, such as GM37v2, providing a sufficient estimated steady-state mean concentration in the cerebrospinal fluid (CSF), sufficient exposure in terms of the area under the curve (AUC), or sufficient estimated binding to the target for alpha-synuclein oligomers in the CSF in order to achieve clinical efficacy. The table below shows the conversion between relevant dosage formulas for a hypothetical patient weighing 70 kg. Table 1: Dosing and conversion between dosage formulations, target binding estimates in cerebrospinal fluid (CSF), and mean steady-state CSF concentrations upon administration by IV intravenous infusion at approximately 28-day intervals. Dosage per kilogram of body weight (mg / kg) The fixed dose for a patient weighing 70 kg (mg) Estimated steady-state mean concentration in cerebrospinal fluid (CSF) (nanomolar) Estimated target binding for alpha-synuclein oligomers in cerebrospinal fluid (CSF) (%) 10 700 * * 15 1050 3 85 20 1400 * * 25 1750 * * 30 2100 6 90 35 2450 * * 40 2800 * * 45 3150 * * 50 3500 * * 55 3850 * * 60 4200 12 95 65 4550 * * 70 4900 * * 75 5250 * * 80 5600 * * 85 5950 * * 90 6300 18 97 95 6650 * * 100 7000 * * 110 7700 * * 120 8400 * * 130 9100 * * * For each dose, the estimated mean Css concentration in cerebrospinal fluid (CSF) and the estimated target binding of aggregated / oligomeric alpha-synuclein in CSF can be calculated as shown in Example 1. Typical dosing regimens are listed in the table below: Method and repetition Dose IV infusion, approximately every 4 weeks (or monthly) 1050 mg or 15 mg / kg IV infusion, approximately every 4 weeks (or monthly) 2100 mg or 30 mg / kg IV infusion, approximately every 4 weeks (or monthly) 4200 mg or 60 mg / kg IV infusion, approximately every 4 weeks (or monthly) 6300 mg or 90 mg / kg For the purposes of this disclosure, the concentrations of antibodies intended for use according to the invention in cerebrospinal fluid (CSF) are assumed to be equal to the concentrations of antibodies reported in interstitial cerebrospinal fluid (ISF). In one formulation, GM37v2 is administered intravenously according to a dosing regimen that achieves the desired therapeutic concentration in the cerebrospinal fluid (CSF) and / or cerebral interstitial fluid (ISF) of a patient. In another formulation, the antibody achieves sufficient concentration to penetrate the brain and exert a therapeutic effect, for example, by binding to aggregated alpha-synuclein and inducing its clearance / inhibition via microglia-dependent and / or microglia-independent mechanisms, and / or reducing alpha-synuclein aggregation, and / or prion-like diffusion between cells. In another embodiment, the therapeutic concentration required for GM37v2 in cerebrospinal fluid (CSF) and / or cerebral interstitial fluid (ISF) could be equal to the concentration capable of achieving and maintaining (after one or more doses) a reduction in alpha-synuclein pooled in ISF and / or CSF of the treated subject of not less than 10-100%, such as 20-90%, 30-80%, 40-70%, 50-60%, or not less than 10%, or not less than 20%, or not less than 30%, or not less than 40%, or not less than 50%, or not less than 60%, or not less than 70%, or not less than 80%, or not less than 85%, or not less than 90%, or not less than 95%. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC50 concentration in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC50 and lower than the estimated IC95 concentration of alpha-synuclein oligomeric in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC85 concentration of alpha-synuclein oligomer and lower than the estimated IC95 concentration in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC85 concentration of alpha-synuclein oligomeric in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC90 concentration of alpha-synuclein oligomeric in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In one embodiment, the dosing regimen achieves a GM37v2 concentration that is higher than the estimated IC95 concentration of alpha-synuclein oligomeric in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In another embodiment, the dosing regimen achieves a concentration of GM37v2 that is capable of achieving and maintaining (after one or more doses) an estimated reduction of more than 50% in alpha-synuclein collected in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In another embodiment, the dosing regimen achieves a concentration of GM37v2 that is capable of achieving and maintaining (after one or more doses) an estimated reduction of over 80% in alpha-synuclein collected in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In another embodiment, the dosing regimen achieves a concentration of GM37v2 that is capable of achieving and maintaining (after one or more doses) an estimated reduction of over 90% in alpha-synuclein collected in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. In another embodiment, the dosing regimen achieves a concentration of GM37v2 that is capable of achieving and maintaining (after one or more doses) an estimated reduction of over 95% in alpha-synuclein collected in the cerebral interstitial fluid (ISF) and / or cerebrospinal fluid (CSF) of the treated subject. These dosing regimens are relevant and applicable to all synovial disorders and prodromal synovial disorders. In particular, these dosing regimens are relevant for the treatment of multiple systemic atrophy (MSA), such as MSA-C, MSA-P, early MSA-P and / or early MSA-C, MSA in patients who are less affected by the disease, or MSA patients who achieve a low UMSARS TS score on first dose, such as <40 (e.g., <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, or (30-35, or 10-30, or 15-30, or 20-30, or 25-30, or 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15). The ultimate dosing regimen is determined based on the estimated mean steady-state concentration required in the cerebrospinal fluid (CSF) necessary to achieve the target binding to alpha-synuclein oligomers in the CSF / brain.Although the precise amount of accumulated alpha-synuclein that needs to be removed from cerebrospinal fluid (CSF) / interstitial fluid (ISF) to modify and / or slow disease progression is not known, no significant difference in CSF alpha-synuclein burden has been observed among different types of synonucleopathies. For example, Tateno et al. showed that CSF alpha-synuclein levels were similar among patients with Lewy body dementia (DLB), Parkinson's disease (PD), and multiple system atrophy (MSA) (Tateno et al., Alzheimer Disorder 2012;26:213–216), suggesting that dosing regimens can be expected to be appropriate for synonucleopathies in general, and thus not limited to specific indications such as Parkinson's disease (PD), DLB, or MSA. Furthermore, dosing regimens are also relevant for patients with prodromal synonucleopathies because these patients have shown indications of altered alpha-synuclein protein processing; for example, Mollenhauer et al. showed that among groups with prodromal synonucleopathies, those treated with anosmia had the lowest mean cerebrospinal fluid (CSF) alpha-synuclein protein levels, while those treated with iRBD had levels intermediate between healthy controls and Parkinson's patients (Mollenhauer et al. Mov Disord. 2019 September; 34(9): 1354–1364). These findings suggest that patients with clinical features of prodromal synonucleopathies already have low CSF alpha-synuclein protein levels, consistent with significant pathological impairment already present during these prodromal phases. Antibodies intended for use in accordance with the invention. The antibodies intended for use in accordance with this invention are bound to an epitope located within positions 112-117. In one embodiment, the invention relates to the monoclonal antibody GM37, or one of its variants (for example, GM37 Variant 1, GM37 Variant 2, GM37 Variant 3), or GM285 intended for use in the treatment of synonucleosis or prodromal synonucleosis. The antibodies GM37, GM37 Variant 1, GM37 Variant 2, and GM37 Variant 3 bind to an epitope located within amino acid positions 112-117 ( Serial ID number : 9 (ILEDMP)( of human alpha-synuclein protein) Serial ID number :10 Specifically, the GM37, GM37 Variant 1, GM37 Variant 2, and GM37 Variant 3 antibodies bind to all 6 amino acids located in that epitope. The GM285 antibody binds to the epitope consisting of amino acids 112-115 (ILED; Serial ID number :19 ) of human alpha-synuclein protein ( Serial ID number :10 ). The terms "anti-alpha-synuclein antibody" or "anti-alpha-synuclein antibody" (used interchangeably) refer to an antibody that binds to the alpha-synuclein protein or a fragment of the alpha-synuclein protein. Specifically, antibodies intended for use under this invention bind to the alpha-synuclein protein amino acid sequence corresponding to sequence identification numbers 9 and / or 19. The term "GM37" refers to an antibody that includes the CDR1-3 integration limiting regions of the heavy chain. Serial identification numbers 1, 2, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 In one of its incarnations, the GM37 antibody can include the variable domain of the heavy chain. Serial ID number :7 and / or the variable range of the light chain Serial ID number :8 For example, the GM37 antibody could be an IgG-type antibody containing a heavy chain consisting of a variable domain. Serial ID number :7 and fixed range Serial ID number :18 With a light series consisting of a variable range Serial ID number :8 And a fixed range of the Kappa type Serial ID number :17 . The term "GM37 variant 1" refers to an antibody that includes the CDR1-3 integration limiting regions of the heavy chain. Serial identification numbers 1, 33, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 In one of its incarnations, the GM37 variant 1 antibody can include the variable domain of the heavy chain. Serial ID number :30 and / or the variable range of the light chain Serial ID number :8 For example, the GM37 variant 1 antibody could be an IgG1 antibody containing a heavy chain consisting of a variable domain. Serial ID number :30 and fixed range Serial ID number :18 With a light series consisting of a variable range Serial ID number :8 And a fixed range of the Kappa type Serial ID number :17 . The term antibody "GM37 variant 2," "GM37v2," or "GM37var2" (used interchangeably) refers to an antibody that includes the CDR1-3 complementation limiting regions of the heavy chain. Serial identification numbers 1, 34, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 In one of the incarnations, the GM37 variant 2 antibody includes the variable heavy chain domain that Serial ID number :31 The variable range of the light chain Serial ID number :8 . For example, the GM37 variant 2 antibody could be an IgG1 antibody that includes the CDR1-3 integration limiting regions of the heavy chain. Serial identification numbers 1, 34, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 . For example, the GM37 variant 2 antibody could be a human IgG1 antibody that includes the CDR1-3 heavy chain integration limiting regions. Serial identification numbers 1, 34, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 . For example, the GM37 variant 2 antibody could be an IgG1 antibody that includes a variable heavy chain domain. Serial ID number :31 and a variable range for the light chain Serial ID number :8 . For example, the GM37 variant 2 antibody could be a human IgG1 antibody that includes a variant heavy chain domain. Serial ID number :31 and a variable range for the light chain Serial ID number :8 . For example, the GM37 variant 2 antibody could be an IgG1 antibody that includes a variable heavy chain domain. Serial ID number :31 and a fixed range for the heavy series Serial ID number :18 With a variable range of light chain Serial ID number :8 A fixed range for the Kappa light series Serial ID number :17 . For example, the GM37 variant 2 antibody could be a human IgG1 antibody that includes a variant heavy chain domain. Serial ID number :31 and a fixed range for the heavy series Serial ID number :18 With a variable range of light chain Serial ID number :8 A fixed range for the Kappa light series Serial ID number :17 . In a preferred embodiment, the GM37 antibody variant 2 is Amlenetug. The term "GM37 variant 3" refers to an antibody that includes the CDR1-3 integration limiting regions of the heavy chain. Serial identification numbers 1, 35, and 3 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 4, 5, and 6 In one of its incarnations, the GM37 variant 3 antibody can include the variable domain of the heavy chain. Serial ID number :32 and / or the variable range of the light chain Serial ID number :8 For example, the GM37 variant 3 antibody could be an IgG1 antibody containing a heavy chain consisting of a variable domain. Serial ID number :32 and fixed range Serial ID number :18 With a light series consisting of a variable range Serial ID number :8 And a fixed range of the Kappa type Serial ID number :17 . The term "GM285" refers to an antibody that includes the CDR1-3 integration limiting regions of the heavy chain. Serial identification numbers 20, 21, and 22 The CDR1-3 integration-determining regions of the light chain are as described within Sequence identification numbers 23, 24, and 25 In one of its incarnations, the GM285 antibody can include the variable domain of the heavy chain. Serial ID number :26 and / or the variable range of the light chain Serial ID number :27 For example, the GM285 antibody could be an IgG1 type antibody containing a heavy chain consisting of a variable domain. Serial ID number :26 and fixed range Serial ID number :28 With a light series consisting of a variable range Serial ID number :27 And a fixed range of the Kappa type Serial ID number :29 . In preferred isoforms, the full-length GM37 antibody, or GM37 Variant 1, GM37 Variant 2, GM37 Variant 3, or GM285, is in an IgG isoform, with the IgG1 isoform being the most preferred, and even more preferred is the human or humanized IgG1 isoform. The most preferred is the human GM37v2 IgG1 antibody. A table that includes sequences Specific amino acids for antibodies directed against alpha-synuclein as used here : Serial ID number: 1 Integrity Determination Area CDR 1 for the GM37 Heavy Series Serial ID number: 2 CDR 2 Integrity Determination Area for GM37 Heavy Series Serial ID number: 3 CDR 3 Integrity Determination Area for GM37 Heavy Series Serial ID number: 4 Integrity Determination Area CDR 1 for the GM37 Light Series Serial ID number: 5 CDR 2 Integrity Determination Area for GM37 Light Series Serial ID number: 6 CDR 3 Integrity Determination Area for GM37 Light Series Serial ID number: 7 Variable range of the GM37 heavy series Serial ID number: 8 Variable range of the GM37 light series Serial ID number: 9 Epitope 112-117 of human alpha-synuclein protein Serial ID number: 10 human alpha-synuclein protein Serial ID number: 11 A-Syn-AAKK-BAP Serial ID number: 12 A-Syn-BAAK-BAP Serial ID number: 13 A-Syn-BBAA-BAP Serial ID number: 14 A-Syn-BBKK-BAP Serial ID number: 15 A-Syn-120-140_Del-BAP Serial ID number: 16 Residues 1-119 of human alpha-synuclein protein Serial ID number: 17 Kappa Light Series Fixed Range Serial ID number: 18 The stable band of the IgG1 heavy chain Serial ID number: 19 The 112-115 seal for GM285 Serial ID number: 20 Integrity Determination Area CDR 1 for the GM285 Heavy Series Serial ID number: 21 Integrity Determination Area CDR 2 for the GM285 Heavy Series Serial ID number: 22 CDR 3 Integrity Determination Area for GM285 Heavy Series Serial ID number: 23 Integrity Determination Area CDR 1 for the GM285 Light Series Serial ID number: 24 CDR 2 Integrity Determination Area for GM285 Light Series Serial ID number: 25 CDR 3 Integrity Determination Area for GM285 Light Series Serial ID number: 26 Variable range of the heavy series for GM285 Serial ID number: 27 Variable range of the GM285 light series Serial ID number: 28 The stable band of the IgG1 heavy chain for GM285 Serial ID number: 29 Kappa GM285 Light Series Fixed Range Serial ID number: 30 GM37 Variant 1 Heavy Series Variable Range Serial ID number: 31 GM37 Variant 2 Heavy Series Variable Range Serial ID number: 32 GM37 Variant 3 Heavy Series Variable Range Serial ID number: 33 Integrity Determination Area CDR 2 for the GM37 Variant 1 Heavy Series Serial ID number: 34 Integrity Determination Area CDR 2 for the GM37 Variant 2 Heavy Series Serial ID number: 35 Integrity Determination Area CDR 2 for the GM37 Variant 3 Heavy Series Serial ID number: 36 The link to 9E4 Serial ID number: 37 Human beta-synuclein Serial ID number: 38 human gamma-synuclein Serial ID number: 39 The homologous counterpart of alpha-synuclein in the baboon monkey Serial ID number: 40 Rat homolog of alpha-synuclein Serial ID number: 41 The homolog of alpha-synuclein in mice Serial ID number: 42 HC Heavy Series for 9E4 Serial ID number: 43 LC Heavy Series for 9E4 sequences Specific amino acids are used here: GFTFSSYAMT (Sequence ID: 1 ) AIRSN GDRTD YADSVKG (Sequence Identification Number: 2 ) AIRSS GDRTD YADSVKG (Sequence Identification Number: 33 ) AIRSQ GDRTD YADSVKG (Sequence Identification Number: 34 ) AIRSH GDRTD YADSVKG (Sequence ID Number: 35 ) AKNWAPFDS (Sequence ID Number: 3 ) ASQSVSSSYLA (Sequence ID Number: 4 ) GASSRAT (Sequence ID Number: 5 ) QQYGSSPWT (Sequence ID Number: 6 ) EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSNGDRTDY ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS (رقم تعريف التسلسل: 7 ) EIVLTQSPGT LSLSPGERAT LSCRASQSVS SSYLAWYQQK PGQAPRLLIY GASSRATGIP DRFSGSGSGT DFTLTISRLE PEDFAVYYCQ QYGSSPWTFG QGTKVEIK (Sequence ID Number: 8 ) EVQLLESGGG LVQPGGSLRL SCAASGFTFS RFTMTWVRQA PGKGLEWVSA ISGSGGGTSY ADSVKGRLTV SRDNSKNTLY LQMNSLRAED TAVYYCAKNW APFDYWGQGT LVTVSS ( Serial ID number 26 ). EIVLTQSPGT LSLSPGERAT LSCRASQSVS RSYLAWYQQK PGQAPRLLIY GASSRATGIP DRFSGSGSGT DFTLTVSRLE PEDFAVYYCQ QYGSSPWTFG QGTKVEIK (Sequence ID Number: 27 ). EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSSGDRTDY ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS (رقم تعريف التسلسل: 30 ) EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSQGDRTDY ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS (رقم تعريف التسلسل: 31 ) EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSHGDRTDY ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS (رقم تعريف التسلسل: 32 ) RTVAAPSVFI FPPSDEQLKS GTASVVCLLN NFYPREAKVQ WKVDNALQSG NSQESVTEQD SKDSTYSLSS TLTLSKADYE KHKVYACEVT HQGLSSPVTK SFNRGEC ( Serial ID number: 17 ) ASTKGPSVFP LAPSSKSTSG GTAALGCLVK DYFPEPVTVS WNSGALTSGV HTFPAVLQSS GLYSLSSVVT VPSSSLGTQT YICNVNHKPS NTKVDKRVEP KSCDKTHTCP PCPAPELLGG PSVFLFPPKP KDTLMISRTP EVTCVVVDVS HEDPEVKFNW YVDGVEVHNA KTKPREEQYN STYRVVSVLT VLHQDWLNGK EYKCKVSNKA LPAPIEKTIS KAKGQPREPQ VYTLPPSREE MTKNQVSLTC LVKGFYPSDI AVEWESNGQP ENNYKTTPPV LDSDGSFFLY SKLTVDKSRW QQGNVFSCSV MHEALHNHYT QKSLSLSPG (رقم تعريف التسلسل: 18 ) AASGFTFSRFTMT (Sequence ID Number: 20 ) AISGSGGGTS YADSVKG (Sequence Identification Number: 21 ) AKNWAPFDY (Sequence ID Number: 22 ) RASQSVSRSYLA (Sequence Identification Number: 23 ) GASSRAT (Sequence ID Number: 24 ) QQYGSSPWT (Sequence ID Number: 25 ) List sequences The full details are below: Sequence list information: DTD version: V1_3 File name: PCT Seq list ST26.xml1294-WO- Program name: WIPO Sequence Software version: 2.3.0 Production date: 2025-02-21 General information: Current application / Intellectual Property Office: WO Current application / applicant reference: 1294-WO-PCT Applicant's Name: H. Lundbeck A / S Applicant's name / language: English Applicant's name / name in Latin characters: H. Lundbeck A / S Title of the invention: Compositions and methods for treating multiple systemic atrophy (MSA) (in Arabic) Total number of sequences: 43 Sequences: Serial number (ID): 1 Length: 10 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.10 Note: CDR1 region for the GM37 heavy series Source, 1.10 Molecule type: protein Living organism, artificial construct The remains: GFTFSSYAMT 10 Serial number (ID): 2 Length: 17 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.17 Note: CDR2 region for the GM37 heavy series Source, 1.17 Molecule type: protein Living organism, artificial construct The remains: AIRSNGDRTD YADSVKG 17 Serial number (ID): 3 Length: 9 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..9 Note: CDR3 region of the GM37 heavy series Source, 1.9 Molecule type: protein Living organism, artificial construct The remains: AKNWAPFDS 9 Serial number (ID): 4 Length: 11 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..11 Note: CDR1 area of ​​the GM37 light series Source, 1.11 Molecule type: protein Living organism, artificial construct The remains: ASQSVSSSYL A 11 Serial number (ID): 5 Length: 7 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..7 Note: CDR2 region of the GM37 light series Source, 1.7 Molecule type: protein Living organism, artificial construct The remains: GASSRAT 7 Serial number (ID): 6 Length: 9 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..9 Note: CDR area 3 for the GM37 light series Source, 1.9 Molecule type: protein Living organism, artificial construct The remains: QQYGSSPWT 9 Serial number (ID): 7 Length: 116 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..116 Note: CDR area for the GM37 heavy series Source, 1.116 Molecule type: protein Living organism, artificial construct The remains: EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSNGDRTDY 60 ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS 116 Serial number (ID): 8 Length: 108 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..108 Note: The GM37 light series Source, 1.108 Molecule type: protein Living organism, artificial construct The remains: EIVLTQSPGT LSLSPGERAT LSCRASQSVS SSYLAWYQQK PGQAPRLLIY GASSRATGIP 60 DRFSGSGSGT DFTLTISRLE PEDFAVYYCQ QYGSSPWTFG QGTKVEIK 108 Serial number (ID): 9 Length: 6 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..6 Note: The epilogue 112-117 Source, 1.6 Molecule type: protein Living organism, artificial construct The remains: ILEDMP 6 Serial number (ID): 10 Length: 140 Molecule type: AA Attributes: Location / Specifiers: Area 1,140 Note, alpha-synuclein Source, 1.140 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDP 120 DNEAYEMPSE EGYQDYEPEA 140 Serial number (ID): 11 Length: 165 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.165 Note, A-Syn-AAKK-BAP Source, 1.165 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGNIAA ATGLVKKDQL AKQNEEGFLQ EGMVNNTDIP 120 VDPENEAYEM PPEEEYQDYE PEAGSAGGSG GLNDIFEAQK IEWHE 165 Serial number (ID): 12 Length: 165 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.165 Note, A-Syn-BAAK-BAP Source, 1.165 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSM AKEGVVAAAE KTKQGVTEAA EKTKEGVLYV GSKTKEGVVH GVATVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL AKQNEEGFLQ EGMVNNTDIP 120 VDPENEAYEM PPEEEYQDYE PEAGSAGGSG GLNDIFEAQK IEWHE 165 Serial number (ID): 13 Length: 162 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.162 Note: A-Syn-BBAA-BAP Source, 1.162 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSM AKEGVVAAAE KTKQGVTEAA EKTKEGVLYV GSKTREGVVQ GVASVAEKTK 60 EQASHLGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDP 120 DNEAYEMPSE EGYQDYEPEA GSAGGSGGLN DIFEAQKIEW HE 162 Serial number (ID): 14 Length: 165 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.165 Note: A-Syn-BBKK-BAP Source, 1.165 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSM AKEGVVAAAE KTKQGVTEAA EKTKEGVLYV GSKTREGVVQ GVASVAEKTK 60 EQASHLGGAV VTGVTAVAQK TVEGAGNIAA ATGLVKKDQL AKQNEEGFLQ EGMVNNTDIP 120 VDPENEAYEM PPEEEYQDYE PEAGSAGGSG GLNDIFEAQK IEWHE 165 Serial number (ID): 15 Length: 141 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..141 Note: A-Syn-120-140_Del-BAP Source, 1.141 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDG 120 SAGGSGGLND IFEAQKIEWH E 141 Serial number (ID): 16 Length: 131 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..131 Note: Amino acids 1-119 of alpha-synuclein Source, 1.131 Molecule type: protein Living organism, artificial construct The remains: MAHHHHHHIE GRMDVFMKGL SKAKEGVVAA AEKTKQGVAE AAGKTKEGVL YVGSKTKEGV 60 VHGVATVAEK TKEQVTNVGG AVVTGVTAVA QKTVEGAGSI AAATGFVKKD QLGKNEEGAP 120 QEGILEDMPV D 131 Serial number (ID): 17 Length: 107 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..107 Note: (The fixed area of ​​the LC light chain) is of the Kappa type. Source, 1.107 Molecule type: protein Living organism, artificial construct The remains: RTVAAPSVFI FPPSDEQLKS GTASVVCLLN NFYPREAKVQ WKVDNALQSG NSQESVTEQD 60 SKDSTYSLSS TLTLSKADYE KHKVYACEVT HQGLSSPVTK SFNRGEC 107 Serial number (ID): 18 Length: 329 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..329 Note: (The fixed region of the heavy chain HC) is of the IgG1 type. Source, 1.329 Molecule type: protein Living organism, artificial construct The remains: ASTKGPSVFP LAPSSKSTSG GTAALGCLVK DYFPEPVTVS WNSGALTSGV HTFPAVLQSS 60 GLYSLSSVVT VPSSSLGTQT YICNVNHKPS NTKVDKRVEP KSCDKTHTCP PCPAPELLGG 120 PSVFLFPPKP KDTLMISRTP EVTCVVVDVS HEDPEVKFNW YVDGVEVHNA KTKPREEQYN 180 STYRVVSVLT VLHQDWLNGK EYKCKVSNKA LPAPIEKTIS KAKGQPREPQ VYTLPPSREE 240 MTKNQVSLTC LVKGFYPSDI AVEWESNGQP ENNYKTTPPV LDSDGSFFLY SKLTVDKSRW 300 QQGNVFSCSV MHEALHNHYT QKSLSLSPG 329 Serial number (ID): 19 Length: 4 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..4 Note: The epithet 112-115 is for GM285 Source, 1.4 Molecule type: protein Living organism, artificial construct The remains: ILED 4 Serial number (ID): 20 Length: 13 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..13 Note: CDR1 region of the GM285 heavy series Source, 1.13 Molecule type: protein Living organism, artificial construct The remains: AASGFTFSRF TMT 13 Serial number (ID): 21 Length: 17 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.17 Note: CDR2 region of the GM285 heavy series Source, 1.17 Molecule type: protein Living organism, artificial construct The remains: AISGSGGGTS YADSVKG 17 Serial number (ID): 22 Length: 9 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..9 Note: CDR3 region of the GM285 heavy series Source, 1.9 Molecule type: protein Living organism, artificial construct The remains: AKNWAPFDY 9 Serial number (ID): 23 Length: 12 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..12 Note: CDR1 area of ​​the GM285 light series Source, 1.12 Molecule type: protein Living organism, artificial construct The remains: RASQSVSRSY LA 12 Serial number (ID): 24 Length: 7 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..7 Note: CDR2 area of ​​the GM285 light series Source, 1.7 Molecule type: protein Living organism, artificial construct The remains: GASSRAT 7 Serial number (ID): 25 Length: 9 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..9 Note: CDR3 area of ​​the GM285 light series Source, 1.9 Molecule type: protein Living organism, artificial construct The remains: QQYGSSPWT 9 Serial number (ID): 26 Length: 116 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..116 Note: VH area for GM285 Source, 1.116 Molecule type: protein Living organism, artificial construct The remains: EVQLLESGGG LVQPGGSSLRL SCAASGFTFS RFTMTWVRQA PGKGLEWVSA ISGSGGGTSY 60 ADSVKGRLTV SRDNSKNTLY LQMNSLRAED TAVYYCAKNW APFDYWGQGT LVTVSS 116 Serial number (ID): 27 Length: 108 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..108 Note: VL area for GM285 Source, 1.108 Molecule type: protein Living organism, artificial construct The remains: EIVLTQSPGT LSLSPGERAT LSCRASQSVS RSYLAWYQQK PGQAPRLLIY GASSRATGIP 60 DRFSGSGSGT DFTLTVSRLE PEDFAVYYCQ QYGSSPWTFG QGTKVEIK 108 Serial number (ID): 28 Length: 329 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..329 Note: The stable region of the IgG1 chain is for GM285. Source, 1.329 Molecule type: protein Living organism, artificial construct The remains: ASTKGPSVFP LAPSSKSTSG GTAALGCLVK DYFPEPVTVS WNSGALTSGV HTFPAVLQSS 60 GLYSLSSVVT VPSSSLGTQT YICNVNHKPS NTKVDKRVEP KSCDKTHTCP PCPAPELLGG 120 PSVFLFPPKP KDTLMISRTP EVTCVVVDVS HEDPEVKFNW YVDGVEVHNA KTKPREEQYN 180 STYRVVSVLT VLHQDWLNGK EYKCKVSNKA LPAPIEKTIS KAKGQPREPQ VYTLPPSREE 240 MTKNQVSLTC LVKGFYPSDI AVEWESNGQP ENNYKTTPPV LDSDGSFFLY SKLTVDKSRW 300 QQGNVFSCSV MHEALHNHYT QKSLSLSPG 329 Serial number (ID): 29 Length: 106 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..106 Note: Kappa series for GM285 Source, 1.106 Molecule type: protein Living organism, artificial construct The remains: TVAAPSVFIF PPSDEQLKSG TASVVCLLNN FYPREAKVQW KVDNALQSGN SQESVTEQDS 60 KDSTYSLSST LTLSKADYEK HKVYACEVTH QGLSSPVTKS FNRGEC 106 Serial number (ID): 30 Length: 116 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..116 Note: The heavy series for GM37 Variant 1 Source, 1.116 Molecule type: protein Living organism, artificial construct The remains: EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSSGDRTDY 60 ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS 116 Serial number (ID): 31 Length: 116 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..116 Note: The heavy series for the GM 37 variant 2 Source, 1.116 Molecule type: protein Living organism, artificial construct The remains: EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSQGDRTDY 60 ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS 116 Serial number (ID): 32 Length: 116 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..116 Note: The heavy series for the GM 37 variant 3 Source, 1.116 Molecule type: protein Living organism, artificial construct The remains: EVQLLESGGG LVQTGGSLRL SCAASGFTFS SYAMTWVRQA PGKGLEWVSA IRSHGDRTDY 60 ADSVKGRFTI SRDNSQNTLY LQMNSLRAED TAVYYCAKNW APFDSWGQGT LVTVSS 116 Serial number (ID): 33 Length: 17 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.17 Note: CDR2 region of the heavy chain for GM37 variant 1 Source, 1.17 Molecule type: protein Living organism, artificial construct The remains: AIRSSGDRTD YADSVKG 17 Serial number (ID): 34 Length: 17 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.17 Note: CDR2 region of the heavy chain for GM37 variant 2 Source, 1.17 Molecule type: protein Living organism, artificial construct The remains: AIRSQGDRTD YADSVKG 17 Serial number (ID): 35 Length: 17 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.17 Note: CDR2 region of the heavy chain for GM37 variant 3 Source, 1.17 Molecule type: protein Living organism, artificial construct The remains: AIRSHGDRTD YADSVKG 17 Serial number (ID): 36 Length: 5 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..5 Note: Link ending 9E4 Source, 1.5 Molecule type: protein Living organism, artificial construct The remains: NEAYE 5 Serial number (ID): 37 Length: 134 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.134 Note: Human beta-synuclein Source, 1.134 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSM AKEGVVAAAE KTKQGVTEAA EKTKEGVLYV GSKTREGVVQ GVASVAEKTK 60 EQASHLGGAV FSGAGNIAAA TGLVKREEFP TDLKPEEVAQ EAAAEEPLIEP LMEPEGESYE 120 DPPQEEYQEY EPEA 134 Serial number (ID): 38 Length: 127 Molecule type: AA Attributes: Location / Specifiers: - Area, 1..127 Note: Human gamma-synuclein Source, 1.127 Molecule type: protein Living organism, artificial construct The remains: MDVFKKGFSI AKEGVVGAVE KTKQGVTEAA EKTKEGVMYV GAKTKENVVQ SVTSVAEKTK 60 EQANAVSEAV VSSVNTVATK TVEEAENIAV TSGVVRKEDL RPSAPQQEGE ASKEKEEVAE 120 EAQSGGD 127 Serial number (ID): 39 Length: 140 Molecule type: AA Attributes: Location / Specifiers: Area 1,140 Note: The analog of alpha-synuclein in the rhesus monkey Source, 1.140 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFIKKDQL GKNEEGAPQE GILQDMPVDP 120 DNEAYEMPSE EGYQDYEPEA 140 Serial number (ID): 40 Length: 140 Molecule type: AA Attributes: Location / Specifiers: Area 1,140 Note: The analogue of alpha-synuclein in rats Source, 1.140 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVTVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGNIAA ATGFVKKDQM GKGEEGYPQE GILEDMPVDP 120 SSEAYEMPSE EGYQDYEPEA 140 Serial number (ID): 41 Length: 140 Molecule type: AA Attributes: Location / Specifiers: Area 1,140 Note: The analogue of alpha-synuclein in mice Source, 1.140 Molecule type: protein Living organism, artificial construct The remains: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVTVAEKTK 60 EQVTNVGGAV VTGVTAVAQK TVEGAGNIAA ATGFVKKDQM GKGEEGYPQE GILEDMPVDP 120 GSEAYEMPSE EGYQDYEPEA 140 Serial number (ID): 42 Length: 446 Molecule type: AA Attributes: Location / Specifiers: - Area, 1.446 Note: HC area for 9E4 Source, 1.446 Molecule type: protein Living organism, artificial construct The remains: EVQLVESGGG LVQPGGSSLRL SCAASGFTFS NYGMSWVRQA PGKGLEWVAS ISSGGGSTYY 60 PDNVKGRFTI SRDNAKNSLY LQMNSLRAED TAVYYCARGG AGIDYWGQGT LVTVSSASTK 120 GPSVFPLAPS SKSTSGGTAA LGCLVKDYFP EPVTVSWNSG ALTSGVHTFP AVLQSSGLYS 180 LSSVVTVPSS SLGTQTYICN VNHKPSNTKV DKRVEPKSCD KTHTCPPCPA PELLGGPSVF 240 LFPPKPKDTL MISRTPEVTC VVVDVSHEDP EVKFNWYVDG VEVHNAKTKP REEQYNSTYR 300 VVSVLTVLHQ DWLNGKEYKC KVSNKALPAP IEKTISKAKG QPREPQVYTL PPSREEMTKN 360 QVSLTCLVKG FYPSDIAVEW ESNGQPENNY KTTPPVLDSD GSFFLYSKLT VDKSRWQQGN 420VFSCSVMHEA LHNHYTQKSL SLSPGK 446 Serial number (ID): 43 Length: 220 Molecule type: AA Attributes: Location / Specifiers: Area 1,220 Note: LC area for 9E4 Source, 1.220 Molecule type: protein Living organism, artificial construct The remains: DIQMTQSPSS LSASVGDRVT ITCKSIQTLL YSSNQKNYLA WFQQKPGKAP KLLIYWASIR 60 KSGVPSRFSG SGSGTDFTLT ISSLQPEDLA TYYCQQYYSY PLTFGGGTKL EIKRTVAAPS 120 VFIFPPSDEQ LKSGTASVVC LLNNFYPREA KVQWKVDNAL QSGNSQESVT EQDSKDSTYS 180 LSSTLTLSKA DYEKHKVYAC EVTHQGLSSP VTKSFNRGEC 220 the end The antibodies intended for use in accordance with this invention may be obtained from any suitable source and, in some embodiments, may be produced in different cell lines, such as in a human cell line, a non-human mammalian cell line, or an insect cell line, for example, in a CHO cell line, HEK cell line, BHK-21 cell line, a mouse cell line (such as a myeloma cell line), a fibrosarcoma cell line, a PER.C6 cell line, an HKB-11 cell line, a CAP cell line, or a human HuH-7 cell line. In one incarnation, the antibody intended for use under the invention is a human antibody. Human monoclonal antibodies directed against alpha-synuclein can be generated using genetically modified or chromosomally modified mice that carry components of the human immune system instead of the mouse immune system. These genetically modified and chromosomally modified mice include those that may be referred to as HuMAb mice and KM mice, respectively. In one embodiment, the antibodies prepared for use under this invention, namely GM37 and its variants GM37 var 1-3 and GM285, are capable of binding to the toxic alpha-synuclein fragments of residues 1-119 / 122 of alpha-synuclein and neutralizing their toxicity (e.g., by extracellularly binding to the alpha-synuclein fragment and thus preventing its uptake by cells). In another embodiment, the antibodies prepared for use under this invention are capable of binding to an epitope located within amino acid positions 112-117 of alpha-synuclein and binding to the toxic alpha-synuclein species in the human brain. In yet another embodiment, the antibodies prepared for use under this invention have an effect of extracellular alpha-synuclein clearance and normalize the abnormal synaptic transmission induced by alpha-synuclein in vivo. In yet another embodiment, the antibodies prepared for use under this invention are also capable of enhancing the appearance of a relevant motor phenotype in a rat model of Parkinson's disease. All these features are described in detail in application WO2017 / 009312. Pharmaceutical formulations and methods of administration A pharmaceutical formulation intended for use in accordance with this invention may include thinners, fillers, salts, buffering agents, detergents (for example, a non-ionic detergent, such as Tween-20 or Tween-80), stabilizers (for example, sugars or protein-free amino acids), preservatives, tissue stabilizers, solvents, and / or other substances suitable for inclusion in a pharmaceutical formulation. In addition, the pharmaceutical formulation may also include other carriers, non-toxic, non-therapeutic, non-antigenic stabilizers, and the like. Formulations may also include slow-metabolizing macromolecules, such as proteins, polysaccharides like chitosan, polylactic acids, polyglycolic acids, copolymers (e.g., functionalized latex cepharose, agarose, cellulose, and the like), polymerized amino acids, amino acid copolymers, and lipid aggregates (e.g., oil droplets or liposomes). Acceptable carriers for pharmaceutical purposes include any and all suitable solvents, dispersing media, coatings, antibacterial and antifungal agents, osmotic pressure agents, antioxidants, absorption retarders, and similar substances that are physiologically compatible with the antibody intended for use in accordance with the invention. Examples of suitable aqueous and non-aqueous carriers that may be used in the pharmaceutical formulations for this invention include water, saline, phosphate-buffered saline, ethanol, dextrose, polyols (such as glycerol, propylene glycol, polyethylene glycol, and similar substances), suitable mixtures thereof, vegetable oils such as olive oil, corn oil, peanut oil, cottonseed oil, or sesame oil, colloidal solutions of carboxymethyl cellulose, tragacanth gum, organic esters such as ethyl oleate, and / or various buffering agents. Other carrier materials are well known in pharmaceutical science and can also be used in this invention. Pharmaceuticalally acceptable carriers include sterile aqueous solutions or dispersion media and sterile powders for the immediate preparation of sterile solutions. The pharmaceutical formulations for this invention may also include, for example, (1) water-soluble antioxidants, such as ascorbic acid, cysteine ​​hydrochloride, sodium bisulfite, sodium metabisulfite, sodium sulfite, and the like; (2) oil-soluble antioxidants, such as ascorbyl palmitate, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), lecithin, propyl gallate, alpha-tocopherol, and the like; and (3) metal chelating agents, such as citric acid, ethylenediaminetetraacetic acid (EDTA), sorbitol, tartaric acid, phosphoric acid, and the like. The pharmaceutical formulations for this invention may also include osmotic pressure agents in the formulations, such as sugars, or polyalcoholic compounds, such as mannitol, sorbitol, glycerol, or sodium chloride. The pharmaceutical formulations for this invention may also contain one or more excipients suitable to the chosen route of administration, such as preservatives, wetting agents, emulsifying agents, dispersing agents, buffering agents, or buffering agents, which may enhance the shelf life or efficacy of the pharmaceutical formulation. The antibodies for this invention may be prepared with carriers that protect the antibody from rapid release, such as in controlled-release formulations, including implants, transdermal patches, and encapsulated delivery systems. These carriers may include gelatin, glyceryl monostearate, glyceryl distearate, biodegradable and biocompatible polymers such as ethylene vinyl acetate, polyanhydrides, polyglycolic acid, collagen, polyorthoesters, polylactic acid alone or in combination with wax, or other materials well known in the field. The methods for preparing these formulations are generally known to specialists in the field. Pharmaceutical formulations for infusion must generally be sterile and stable under manufacturing and storage conditions. The formulation may be a solution, microemulsion, liposome, or other structured form suitable for achieving a high concentration of the drug. The carrier may be an aqueous or non-aqueous solvent or dispersing medium containing, for example, water, ethanol, polyols (such as glycerol, propylene glycol, polyethylene glycol, and the like), suitable mixtures thereof, vegetable oils such as olive oil, or organic esters such as ethyl oleate. Sterile solutions for infusion can be prepared by incorporating the required amount of active antibody into a suitable solvent with one or more components, for example, as listed above, followed by aseptic filtration. Dispersion media are generally prepared by incorporating the active antibody into a sterile carrier liquid containing the primary dispersion medium and other required components, for example, those listed above. For sterile powders intended for sterile solutions, preparation methods include, for example, vacuum drying and freeze-drying (lyophilization), which produce a powder containing the active ingredient plus any desired additional components from a solution previously sterile by filtration. The formulations can be formulated in unit dose form to facilitate administration and standardize the dosage. The term "unit dose form," as used here, refers to convenient units used as standardized doses for the patients being treated; each unit contains a predetermined amount of the active antibody sufficient to achieve the desired therapeutic effect, in conjunction with the required pharmaceutical excipients. In one particular form, the pharmaceutical formulation is given by intravenous infusion. Specific liquid pharmaceutical formulations In one aspect, the antibody intended for use according to the invention is formulated as a liquid pharmaceutical preparation and administered by intravenous infusion. In one aspect, this invention provides for the use of a liquid pharmaceutical formulation containing a full-length IgG1 anti-alpha-synuclein monoclonal antibody at a concentration of approximately 20-230 mg / ml, such as 25-225 mg / ml, where the said antibody includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number : 6 ; The formulation also includes a buffering agent, a pharmaceutically acceptable stress-reducing agent, and a pharmaceutically acceptable surfactant. The pH of the formulation is between 4.5 and 7.5, such as between 5.0 and 7.0, or between 5.5 and 6.5, such as 6.0. In a preferred embodiment, the liquid pharmaceutical formulation prepared for use according to the invention is a stable liquid pharmaceutical formulation. In a preferred embodiment, the liquid pharmaceutical formulation is a low-viscosity liquid pharmaceutical formulation. In a preferred embodiment, the liquid pharmaceutical formulation is a stable, low-viscosity liquid pharmaceutical formulation. In a preferred embodiment, the liquid pharmaceutical formulation is suitable for clinical use and safe for patients who need to administer / receive doses of it. In certain formulations, the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation also includes a variable heavy chain domain consisting of Serial ID number : 31 A variable range for a light chain consisting of Serial ID number : 8 In more specific terms, the anti-alpha-synuclein monoclonal antibody also includes a fixed heavy chain domain as defined in Serial ID number :18 And a fixed range for the Kappa-type light chain as defined in Serial ID number :17 . In some formulations, the liquid pharmaceutical formulation includes an anti-alpha-synuclein monoclonal antibody at a concentration greater than 20 mg / ml, and in some formulations, at a concentration less than 230 mg / ml. In additional formulations, the concentration of the anti-alpha-synuclein monoclonal antibody in the pharmaceutical formulation ranges from 20-225 mg / ml, or 20-220 mg / ml, or 20-215 mg / ml, or 20-210 mg / ml, or 20-205 mg / ml, or 20-200 mg / ml, or 20-195 mg / ml, or 20-190 mg / ml, or 20-185 mg / ml, or 20-180 mg / ml, or 20-175 mg / ml, or 20-170 mg / ml, or 20-165 mg / ml, or 20-160 mg / ml, or 20-155 mg / ml, or 20-150 mg / mL, or 20-145 mg / mL, or 20-140 mg / mL, or 20-135 mg / mL, or 20-130 mg / mL, or 20-125 mg / mL, or 20-120 mg / mL, or 20-115 mg / mL, or 20-110 mg / mL, or 20-105 mg / mL, or 20-100 mg / mL, or 20-95 mg / mL, or 20-90 mg / mL, or 20-85 mg / mL, or 20-80 mg / mL, or 20-75 mg / mL, or 20-70 mg / mL, or 20-65 mg / mL, or 20-60 mg / ml, or 20-55 mg / ml, or 20-50 mg / ml, or 20-45 mg / ml, or 20-40 mg / ml, or20-35 mg / ml, or 20-30 mg / ml, or 20-25 mg / ml, or 25-230 mg / ml, or 30-230 mg / ml, or 35-230 mg / ml, or 40-230 mg / ml, or 45-230 mg / ml, or 50-230 mg / ml, or 55-230 mg / ml, or 60-230 mg / ml, or 65-230 mg / ml, or 70-230 mg / ml, or 75-230 mg / ml, or 80-230 mg / ml, or 85-230 mg / ml, or 90-230 mg / ml, or 95-230 mg / ml, or 100-230 mg / ml, or 105-230 mg / ml, or 110-230 mg / ml, or 115-230 mg / ml, or 120-230 mg / ml, or 125-230 mg / ml, or 130-230 mg / ml, or 135-230 mg / ml, or 140-230 mg / ml, or 145-230 mg / ml, or 150-230 mg / ml, or 155-230 mg / ml, or 160-230 mg / ml, or 165-230 mg / ml, or 170-230 mg / ml, or 175-230 mg / ml or 180-230 mg / ml, or 185-230 mg / ml, or 190-230 mg / ml, or 195-230 mg / ml, or 200-230 mg / ml, or 205-230 mg / ml, or 210-230 mg / ml, or 215-230 mg / ml, or 220-230 mg / ml, or 225-230 mg / ml, or 25-225 mg / ml, or 30-220 mg / ml, or 35-215 mg / ml, or 40-210 mg / ml, or 45-205 mg / ml, or 50-200 mg / ml, or 55-195 mg / ml, or 60-190mg / mL, or 65-185 mg / mL, or 70-180 mg / mL, or 75-175 mg / mL, or 80-170 mg / mL, or 85-165 mg / mL, or 90-160 mg / mL, or 95-155 mg / mL, or 100-150 mg / mL, or 105-145 mg / mL, or 110-140 mg / mL, or 115-135 mg / mL, or 120-130 mg / mL; including all values ​​falling within any of these limits. In certain formulations, the liquid pharmaceutical formulation contains an anti-alpha-synuclein monoclonal antibody at a concentration of approximately 50 mg / mL. In other specific formulations, the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation has a concentration of approximately 53 mg / ml. In some formulations, the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation has a concentration within + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, or + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, + / - 1.5%, + / - 1%, + / - 0.75%, + / - 0.5%, + / - 0.25%, or + / - 0.1%.For example + / - 0.05%, or + / - 0.025%, or + / - 0.01%, or + / - 0.0075%, or + / - 0.005%, or + / - 0.0025%, or + / - 0.001%, or + / - 0.0005%. In some embodiments of this invention, the preservative is a single preservative or a mixture of preservatives. In another embodiment, the preservative is chosen from the preservatives of acetate, citrate, tartrate, histidine, glutamate, phosphate, tris, glycine, bicarbonate, succinate, sulfate, nitrate, or any mixture thereof. In further embodiments, the preservatives are chosen from sodium phosphate, histidine (such as L-histidine), citric acid, sodium citrate, sodium acetate, or any mixture thereof. In one specific embodiment, the preservative is the preservative of histidine (such as L-histidine) or a mixture of histidine preservatives. Histidine preventatives can be selected from among histidine preventatives or mixtures thereof, such as histidine, L-histidine, L-histidine hydrochloride, L-histidine monohydrochloride, L-histidine monohydrate, L-histidine monohydrate monohydrochloride, or mixtures thereof. In one preferred formulation, the histidine preventative is a mixture of L-histidine and L-histidine monohydrochloride.In some preferred embodiments of the liquid pharmaceutical formulation, the buffering agent is present at a concentration ranging from 10-60 mM, such as 15-55 mM, or 20-50 mM, or 20-45 mM, or 20-40 mM, such as 25-40 mM, or 10-40 mM, or 15-35 mM, or 20-30 mM, or 25 mM. In some formulations, the buffering agent in the liquid pharmaceutical formulation has a concentration within a range of + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, or + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, + / - 1.5%, + / - 1%, + / - 0.75%, + / - 0.5%, + / - 0.25%, + / - 0.1%, + / - 0.05%, + / - 0.025%, or + / - 0.01%. + / - 0.0075%, or + / - 0.005%, or + / - 0.0025%, or + / - 0.001%, or + / - 0.0005%. In one embodiment, the pH of the liquid pharmaceutical formulation intended for use according to the invention is within a range of approximately 4.5 to approximately 7.5, such as between 4.5 and approximately 6.5, such as 5.0 and 6.5, or such as between approximately 5.5 and approximately 6.5, for example, between 5.7 and 6.4, or between 5.8 and 6.3, or between 5.9 and 6.2. In another embodiment, the liquid pharmaceutical formulation has a pH of 5.5, or 5.6, or 5.7, or 5.8, or 5.9, or 6.0, or 6.1, or 6.2, or 6.3, or 6.4, or 6.5, or 7.0. Histidine buffers (such as L-histidine) are an example of buffering agents that may be included in a liquid pharmaceutical formulation to maintain the pH within this range. In a preferred formulation, the pH of the liquid pharmaceutical formulation is 6.0. In some formulations, the liquid pharmaceutical formulation has a pH within a range of + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, or + / - 1.5%, or like + / - 1%, or like + / - 0.75%, or like + / - 0.5%, or like + / - 0.25%, or like + / - 0.1%, or like + / - 0.05%, or like + / - 0.025%, or like + / - 0.01%, or like + / - 0.0075%, or like + / - 0.005%, or like + / - 0.0025%, or like + / - 0.001%, or like + / - 0.0005%. In one embodiment, the surfactant in the liquid pharmaceutical formulation prepared for use in accordance with the invention is a non-ionic surfactant.In additional embodiments, the surfactant is chosen from the group consisting of polysorbates (e.g., polysorbate 20 and polysorbate 80); poloxamer (e.g., poloxamer 188); Triton; Triton X-100; sodium dodecyl sulfate (SDS); sodium lauryl sulfate; sodium octyl glycoside; lauryl-, myristyl-, linoleyl-, or stearyl-sulfobetaine compounds; lauryl-, myristyl-, linoleyl-, or stearyl-sarcosine compounds; and linoleyl-, myristyl-, or cetyl-betaine compounds. Loramidopropyl-, cocamidopropyl-, linoleimidopropyl-, myristamidopropyl-, palmidopropyl-, or isostearamidopropyl-betane compounds (e.g., loramidopropyl); myristamidopropyl-, palmidopropyl-, or isostearamidopropyl dimethylamine compounds; sodium methylcocoyl, or disodium methyloleate taurate; as well as polyethylene glycol, polypropylene glycol, and ethylene glycol and propylene glycol copolymers.In one specific embodiment, the pharmaceutically acceptable surfactant in the liquid pharmaceutical formulation is polysorbate 80, also known as Tween 80. In some preferred embodiments of the liquid pharmaceutical formulation, the surfactant is present in amounts ranging from 0.001% to 0.10% (w / v), such as 0.005% and 0.08% (w / v), or such as 0.008% and 0.06% (w / v), or such as 0.01% and 0.05% (w / v), or such as 0.015% and 0.05% (w / v), or such as 0.01% and 0.05% (w / v), or such as 0.01% and 0.03% (w / v), or such as 0.02% (w / v). In some formulations, the surfactant in the liquid pharmaceutical formulation has a concentration within + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, or + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, + / - 1.5%, + / - 1%, + / - 0.75%, + / - 0.5%, + / - 0.25%, + / - 0.1%, + / - 0.05%, + / - 0.025%, or + / - 0.01%, or like + / - 0.0075%, or like + / - 0.0.05%, or like + / - 0.0025%, or like + / - 0.001%, or like + / - 0.0005%. In one embodiment, the stabilizing agent in the liquid pharmaceutical formulation prepared for use according to the invention is chosen from mannitol, sorbitol, lactose, dextrose, trehalose, sodium chloride, potassium chloride, glycerol, or glycerol. In one specific embodiment, the stabilizing agent is a suitable salt such as sodium chloride (NaCl). In another specific embodiment, the stabilizing agent in the liquid pharmaceutical formulation is sodium chloride (NaCl). In some preferred embodiments of the liquid pharmaceutical formulation, the tonic is present in a concentration ranging from 10-150 mM, such as 20-140 mM, or 30-130 mM, or 40-120 mM, or 50-110 mM, or 60-110 mM, or 70-110 mM, or 80-110 mM, or 90-110 mM, or about 100 mM.In some formulations, the concentration of the tensile agent in the liquid pharmaceutical formulation is within a range of + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, or + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, + / - 1.5%, + / - 1%, + / - 0.75%, + / - 0.5%, + / - 0.25%, + / - 0.1%, + / - 0.05%, + / - 0.025%, or + / - 0.01%. + / - 0.0075%, or + / - 0.005%, or + / - 0.0025%, or + / - 0.001%, or + / - 0.0005%. In one embodiment, the liquid pharmaceutical formulation prepared for use pursuant to the invention also includes a bulking agent, which is chosen from sugars and polyols (such as sucrose, trehalose, glucose, lactose, sorbitol, mannitol, and glycerol); amino acids (such as arginine, aspartic acid, glutamic acid, lysine, glycine, glutamate, histidine, methionine, or alanine); or polymers and proteins (such as gelatin, PVP, PLGA, PEG, dextran, cyclodextrin and its derivatives, starch derivatives, HSA, or BSA). In one specific embodiment, the bulking agent is chosen from arginine, glutamate, sucrose, glycine, or sorbitol. In one specific embodiment, the bulking agent is sucrose.In some preferred embodiments of the liquid pharmaceutical formulation, there is a volume-increasing agent with a concentration ranging from 20-200 mM, such as 25-180 mM, or 30-170 mM, or 35-160 mM, or 40-150 mM, or 45-140 mM, or 50-130 mM, or 60-130 mM, or 65-120 mM, or 70-120 mM, or 75-120 mM, or 80-110 mM, or 85-110 mM, or 90-110 mM, or 95-110 mM, or 95-105 mM, or 100 mM. In some formulations, the bulking agent in the liquid pharmaceutical formulation has a concentration within + / - 30% of the stated values, such as + / - 25%, + / - 20%, + / - 15%, or + / - 10% of the stated values, such as + / - 8%, + / - 6%, + / - 5%, + / - 4%, + / - 3%, + / - 2.5%, + / - 2%, + / - 1.5%, + / - 1%, + / - 0.75%, + / - 0.5%, + / - 0.25%, + / - 0.1%, + / - 0.05%, + / - 0.025%, or + / - 0.01%. + / - 0.0.075%, or like + / - 0.005%, or like + / - 0.0025%, or like + / - 0.001%, or like + / - 0.0005%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, the histidine buffer, and sodium chloride (NaCl) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 10-60 mM of histidine buffer and 10-150 mM of sodium chloride (NaCl) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synoclane monoclonal antibody, GM37v2, 20-30 mM of histidine buffer and 90-110 mM of sodium chloride (NaCl) at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer and 100 mM of sodium chloride (NaCl) at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer and 100 mM of sodium chloride (NaCl) at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25%, or + / - 0.1%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, the histidine buffer, and polysorbate 80 (Tween 80) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, and 10-60 mM of histidine buffer and polysorbate 80 (Tween 80) in amounts ranging from 0.001% to 0.10% (w / v), at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synoclane monoclonal antibody, GM37v2, and 20-30 mM of histidine buffer and polysorbate 80 (Tween 80) in amounts ranging from 0.01% to 0.03% (w / v), at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, and 25 mM of the histidine buffer and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, and 25 mM of histidine buffer and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25%, or + / - 0.1%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, the histidine buffer, sodium chloride (NaCl) and polysorbate 80 (Tween 80) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 10-60 mM of histidine buffer, 10-150 mM of sodium chloride (NaCl) and polysorbate 80 (Tween 80) in amounts ranging from 0.001% to 0.10% (w / v), at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 20-30 mM of histidine buffer, 90-110 mM of sodium chloride (NaCl) and polysorbate 80 (Tween 80) in amounts ranging from 0.01% to 0.03% (w / v), at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl) and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl) and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25%, or + / - 0.1%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, histidine buffer, sodium chloride (NaCl) and sucrose at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 10-60 mM of histidine buffer, 10-150 mM of sodium chloride (NaCl) and 20-200 mM of sucrose, at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 20-30 mM of histidine buffer, 90-110 mM of sodium chloride (NaCl) and 90-110 mM of sucrose, at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl) and 100 mM of sucrose, at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl) and 100 mM of sucrose, at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25%, or + / - 0.1%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, the histidine buffer, sucrose and polysorbate 80 (Tween 80) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 10-60 mM of histidine buffer, 20-200 mM of sucrose and polysorbate 80 (Tween 80) in amounts ranging from 0.001% to 0.10% (w / v), at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synoclane monoclonal antibody, GM37v2, 20-30 mM of histidine buffer, 90-110 mM of sucrose and polysorbate 80 (Tween 80) in amounts ranging from 0.01% to 0.03% (w / v), at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sucrose and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sucrose and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25%, or + / - 0.1%. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes the anti-alpha-synuclein monoclonal antibody, GM37v2, histidine buffer, sodium chloride (NaCl), sucrose and polysorbate 80 (Tween 80) at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 20-230 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 10-60 mM of histidine buffer, 10-150 mM of sodium chloride (NaCl), 20-200 mM of sucrose and polysorbate 80 (Tween 80) in amounts ranging from 0.001% to 0.10% (w / v), at a pH within the range of 4.5-7.5. In one embodiment, the liquid pharmaceutical formulation prepared for use according to the invention includes 40-60 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 20-30 mM of histidine buffer, 90-110 mM of sodium chloride (NaCl), 90-110 mM of sucrose and polysorbate 80 (Tween 80) in amounts ranging from 0.01% to 0.03% (w / v), at a pH within the range of 5.5-6.5. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl), 100 mM of sucrose and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation prepared for use in accordance with the invention includes 53 mg / ml of the anti-alpha-synuclein monoclonal antibody, GM37v2, 25 mM of histidine buffer, 100 mM of sodium chloride (NaCl), 100 mM of sucrose and polysorbate 80 (Tween 80) in an amount of 0.02% (w / v), at a pH of 6.0 or within the range of + / - 30% of the values ​​stated, such as + / - 25%, or + / - 20%, or + / - 15%, or + / - 10%, or + / - 5%, or + / - 1%, or + / - 0.5%, or + / - 0.25% or + / - 0.1%. In certain embodiments, the liquid pharmaceutical formulation prepared for use according to the invention is presented in 20 ml vials, each vial containing approximately 1000-1060 mg of GM37v2, such as approximately 1060 mg. Synonuclear disorders and prodromal synonuclear disorders Cynopathies refer to disorders characterized by the presence of abnormal collections of alpha-synuclein protein within neurons known as Lewy bodies. Cynopathies include Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), diffuse Lewy body disease (DLB) (also known as dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease (CAPD), autonomic nervous system failure (PAF), and multiple system atrophy (MSA; for example, cerebellar olivary atrophy, black striatal degeneration, and Shay-Draeger syndrome)). In one respect, this invention provides suitable dosing regimens for the treatment of syncytia disorders, such as Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and pure autonomic nervous system failure and multiple system atrophy (MSA).In one preferred incarnation, synopathy is Parkinson's disease (PD). In another preferred incarnation, synopathy is dementia with Lewy bodies (DLB). And in yet another preferred incarnation, synopathy is multiple systemic atrophy (MSA). In another preferred incarnation, the patient undergoing treatment for multiple systemic atrophy (MSA) has MSA-C. In another preferred incarnation, the patient undergoing treatment for MSA has MSA-P. In yet another preferred incarnation, the patient undergoing treatment for MSA has clinically probable or likely MSA-C. In yet another preferred incarnation, the patient undergoing treatment for MSA has clinically probable or likely MSA-P. In another preferred incarnation, the person undergoing treatment for multiple systemic atrophy (MSA) has early-stage MSA. In another similar incarnation, the person undergoing treatment for MSA has early-stage MSA. In yet another similar incarnation, the person undergoing treatment for MSA has early-stage MSA. In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein.In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when giving the first dose of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). In another preferred embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) is diagnosed with MSA-C and receives a total UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein.In another similar incarnation, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug).In another similar embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when giving the first dose of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). On the other hand, this invention provides appropriate dosing regimens for treating prodromal synopathies in a patient at risk of developing a synopathy, which can be identified by the presence of one or more clinical signs of prodromal synopathies. These clinical signs of prodromal synopathies can be selected from REM sleep behavior disorder such as isolated RBD (iRBD), olfactory disorder such as anosmia, abnormal cognitive performance on neuropsychological tests, mild motor dysfunction or abnormal motor performance assessed by objective tests, color vision disorder, autonomic nervous system disorders (such as constipation, urinary symptoms, erectile dysfunction, or orthostatic hypotension), reduced black dopaminergic binding in the striatum and substantia nigra (abnormal DAT-SPECT), seborrheic dermatitis, or a genotype associated with an increased risk of phenotypic transformation such as mutations in the glucocerebrosidase enzyme (encoded by the GBA gene). In some manifestations of these aspects, the individual undergoing treatment is identified as exhibiting signs of synonucleosis or prodromal synonucleosis in the form of abnormal accumulation or deposition of alpha-synuclein in the central nervous system. In certain manifestations, the individual undergoing treatment is identified by in vivo imaging of alpha-synuclein (e.g., in the brain) using methods including positron emission tomography (PET), single-photon emission computed tomography (SPECT), near-infrared photometry (NIR), magnetic resonance imaging (MRI), dopamine transporter imaging (DAT), or substantia nigra ultrasound. In some incarnations, the person undergoing treatment is identified as exhibiting signs of synonucleosis or prodromal synonucleosis by measuring the level of alpha-synuclein in a sample of blood, plasma, or cerebrospinal fluid (CSF) obtained from the person undergoing treatment and comparing the measured alpha-synuclein level in the person undergoing treatment to a reference standard, where the difference or similarity between the level of alpha-synuclein in the blood, plasma, or CSF sample and the reference standard relates to the level of alpha-synuclein in the brain of the person undergoing treatment.Alpha-synuclein levels can be assessed using field-established methods, including, for example, alpha-synuclein analysis by one or more selected techniques such as Western blot, immunoprecipitation, enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA), fluorescence-activated cell sorting (FACS), two-dimensional gel electrophoresis, mass spectrometry (MS), matrix-assisted time-of-flight laser desorption / ionization mass spectrometry (MALDI-TOF), surface-enhanced time-of-flight laser desorption / ionization mass spectrometry (SELDI-TOF), high-performance liquid chromatography (HPLC), fast proteolytic liquid chromatography (FPLC), multidimensional liquid chromatography (LC) followed by tandem mass spectrometry (MS / MS), or laser densitometry. In some incarnations, the person undergoing treatment was identified through the appearance of symptoms of synovial disorders or prodromal synovial disorders via methods and criteria recognized in the field. Recently, new diagnostic criteria for MSA, titled "The Movement Disorder Society Criteria for the Diagnosis of Multiple System Atrophy," were published by Wenning et al. and are incorporated here by reference (Wenning et al., Movement Disorders, 2022, Vol. 37, No. 6, pp. 1131–1148). These new criteria describe "probable prodromal MSA research criteria" that can be used to identify a patient with prodromal syncytia. Parkinson's disease PD ) Parkinson's disease (PD) is a syncytiopathic disorder. There are no well-defined diagnostic criteria for PD; however, there is a combination of symptoms and diagnostic tests that can be used to support its diagnosis. Reaching a definitive diagnosis of Parkinson's disease, especially in its early stages, is challenging, but a skilled practitioner can reasonably conclude that a patient has PD using clinical assessment tools. In some manifestations, a diagnosis of PD may be based on the presence of at least two of the four main symptoms of PD: a) Trembling or shaking b) Slowness of movement, also called slowing of movement c) Stiffness or rigidity in the arms, legs, or trunk d) Balance problems with the possibility of falling, also called postural instability. Imaging techniques such as magnetic resonance imaging (MRI), brain ultrasound, PET scans, and / or single-photon emission computed tomography (SPECT), such as dopamine transporter scanning (DaTscan), may also be helpful in supporting the diagnosis of PD. Dementia with Lewy bodies DLB ) Lewy body dementia (LBD) is a type of synovial disorder involving progressive dementia that leads to a decline in thinking, reasoning, and cognitive functions. LBD is often difficult to diagnose because its early symptoms can resemble those of Alzheimer's disease or other psychiatric conditions. There are no definitive diagnostic criteria, but some of the core clinical features of LBD include dementia, movement / parkinsonian problems, cognitive fluctuations, visual hallucinations, and REM sleep behavior disturbances. Supporting clinical features include hypersensitivity to antipsychotics, falls or fainting spells, severe autonomic nervous system dysfunction (such as blood pressure maintenance, urinary incontinence, constipation, and loss of smell), and personality and mood changes (depression, apathy, and anxiety). A diagnosis of Lewy body dementia requires a progressive decline in thinking ability, in addition to at least two of the following: a) Reversing the level of alertness and thinking functions b) Recurrent visual hallucinations c) Parkinsonian symptoms d) REM (rapid eye movement) sleep behavior disorder Dysfunction of the autonomic nervous system, which includes unstable blood pressure and heart rate, impaired regulation of body temperature, sweating, and related signs and symptoms, supports the diagnosis of Lewy body dementia, as well as sensitivity to antipsychotic drugs. Physical and neurological examinations, along with other tests, can help differentiate DLB from other conditions and support a diagnosis of DLB. Qualitative testing may include positron emission tomography (PET) or single-photon emission computed tomography (SPECT) scans, which show reduced dopamine transporter (DAT) binding in the basal ganglia (a brain region), or myocardial scintigraphy using iodine. 123 An abnormal iodine-MIBG test showing impaired sympathetic cardiac innervation, or a sleep study confirming a REM sleep behavior disorder without loss of muscle tone. Multiple systemic atrophy ( MSA ) Multiple system atrophy (MSA) is the most rapidly progressing of the synaptic nephropathies, a group of disorders characterized by abnormal deposition of alpha-synuclein protein in the central nervous system and peripheral autonomic nervous system. In this context, the term MSA refers to all types of MSA, such as parkinsonian-type MSA-P or cerebellar-type MSA-C. MSA is sometimes referred to as cerebellar-olivary atrophy, progressive autonomic failure with multiple system atrophy, black striatal degeneration, or Shay-Draiger syndrome. This invention also provides dosing regimens for the treatment of MSA at all stages of its development, including prodromal, early, intermediate, and advanced stages, and all stages in between. Diagnosing multiple system atrophy (MSA) can be challenging because certain signs and symptoms of MSA, such as muscle rigidity and gait instability, are also present in other disorders, such as Parkinson's disease. Appropriate clinical examination, along with various autonomic nervous system tests and imaging studies, may help determine whether the diagnosed condition is likely MSA or probable MSA. Examples of clinical methods that may be helpful in supporting the diagnosis of MSA in patients suspected of having MSA include structural and functional brain imaging, sympathetic neuroimaging, autonomic nervous system testing, olfactory testing, sleep studies, urinary evaluation, dysphagia assessment, cognitive assessments, skin biopsy, retinal biomarkers, blood and / or cerebrospinal fluid biomarkers, and genetic testing. For example, the diagnosis of possible or probable MSA can be facilitated based on what are known as Gilman's criteria (Gilman et al., Neurology. 2008 Aug 26; 71(9): 670–676). In some incarnations, the person undergoing treatment is likely to have MSA, which can be identified by: a) Autonomic nervous system failure involving urinary incontinence or orthostatic hypotension within 3 minutes of standing by at least 30 mmHg systolic or 15 mmHg diastolic pressure; and b) Parkinsonism poorly responsive to levodopa (bradykinesia with rigidity, tremor, or postural instability); or c) Cerebellar syndrome (gait ataxia with cerebellar dysarthria, limb ataxia, or cerebellar eye movement disorder). In some incarnations, the person undergoing treatment is likely to have MSA, which can be identified by: a) Parkinsonism (slowness of movement with rigidity, tremor, or postural instability); or b) Cerebellar syndrome (gait ataxia with cerebellar dysarthria, limb ataxia, or cerebellar oculomotor disorder); and c) The presence of at least one feature indicative of autonomic nervous system dysfunction (urinary urgency or unexplained urinary frequency, incomplete bladder emptying, erectile dysfunction in males, or a marked decrease in orthostatic blood pressure that does not meet the criteria for a weighted MSA); and d) The presence of at least one of the following characteristics: In cases of possible MSA-P or MSA-C: A. Babinski's sign with hyperreflexia b. Creaking In possible MSA-P cases: C. Rapidly Progressive Parkinsonism Poor response to levodopa treatment e. Postural instability within 3 years of the onset of motor symptoms and gait ataxia, cerebellar dysarthria, limb ataxia, or cerebellar oculomotor dystonia Z. Dysphagia within 5 years of the onset of motor symptoms H. Atrophy of the pituitary gland, or the middle cerebellar peduncle, or the pons, or the cerebellum, is seen on magnetic resonance imaging. T. Metabolic deficiency in the pituitary gland, brainstem, or cerebellum is shown in positron emission tomography using fluorodeoxyglucose (FDG-PET) In possible MSA-C cases: Y. Parkinsonism (slowness of movement and rigidity) K. Atrophy of the pituitary gland, or the middle cerebellar peduncle, or the pons, is seen on MRI. L. Metabolic deficiency in the endothelium is shown in FDG-PET imaging. M. Loss of presynaptic black striatal dopaminergic innervation as seen on single-photon emission computed tomography (SPECT) or PET imaging. Currently, a definitive diagnosis of MSA can only be confirmed post-mortem through proof of: a) The presence of abundant and widespread alpha-synuclein-positive glial cytoplasmic inclusions in the brain; and / or b) The presence of neurodegenerative changes in the stria nigra or olivary-pontine tract. In a preferred incarnation, the person undergoing treatment for MSA disease is also infected with MSA-C. In a preferred embodiment, a person undergoing treatment for MSA also receives a total UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, 20-25, or 10-20, or 15-20, or 10-15 when giving the first dose of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). In a preferred embodiment, a person undergoing treatment for MSA also receives a total UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). In a preferred embodiment, a person undergoing treatment for MSA is also diagnosed with MSA-C and has an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when giving the first dose of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug).In a preferred embodiment, a person undergoing treatment for MSA is also diagnosed with MSA-C and has an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). Recently, new diagnostic criteria for MSA entitled "The Movement Disorder Society Criteria for the Diagnosis of Multiple System Atrophy" were published by Wenning et al and incorporated here by reference (Wenning et al, Movement Disorders, 2022, Vol. 37, No. 6, pp. 1131–1148). These criteria include a clinically confirmed diagnosis of MSA and a clinically probable diagnosis of MSA: MSA-C is characterized by a predominance of cerebellar symptoms. These cerebellar dysfunction symptoms often manifest as gait ataxia, limb ataxia, cerebellar dysarthria, and / or eye movement disorders such as dyspnea, blink interferences, and / or ocular dyspnea. MSA-P is characterized by a predominance of parkinsonian features. These include bradykinesia, rigidity, irregular postural tremor and / or abnormal postural postures (excessive forward trunk curvature, PISA syndrome, and disproportionate forward flexion of the neck). The term "early MSA" refers to patients who are less affected by the disease in its clinical stage. These MSA patients, in this context, score low on any of the UMSARS scales, such as mUMSARS, aUMSARS, UMSARS TS, UMSARS Part 1, or UMSARS Part 2. In preferred incarnations, the term early MSA means that at the start of treatment, the patient has an overall UMSARS TS score of less than 40, such as less than 39, less than 38, less than 37, less than 36, less than 35, less than 34, less than 33, less than 32, less than 31, less than 30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25. 20-25, or 10-20, or 15-20, or 10-15. Rapid eye movement sleep behavior disorder (RBD ) REM Rapid eye movement (REM) sleep behavior disorder is one of the early manifestations of synoclean disorders. REM REM sleep behavior disorder is characterized by "dream-like" behavior and is diagnosed by video sleep studies (vPSG), which show a loss of the muscle relaxation that normally accompanies REM sleep. Like clinically isolated RBD (iRBD) (formerly sometimes referred to as idiopathic RBD), REM RBD is the most reliable clinical sign of prodromal synoclean disorders, a group of neurodegenerative disorders that includes Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). In the vast majority of individuals with REM sleep behavior disorder (iRBD), such as iRBD, synonucleosis is diagnosed within 20 years of the onset of iRBD, such as within 3 years, or within 5 years, or within 8 years, or within 16 years.Therefore, the patient population with REM rapid eye movement (RBD) sleep behavior disorder could represent an ideal group for administering the antibodies prepared for use according to the invention with the aim of modifying the progression of syncylin-associated neurodegeneration, i.e., to obtain a disease-modifying therapy that delays or prevents the apparent transition to overt syncylinopathy. The diagnosis of RBD may be based on certain consensus criteria, such as those established by the International Classification of Sleep Disorders (ICSD-3), the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), or the American Academy of Sleep Medicine (AASM) Sleep and Associated Event Recording Guide. Confirmation of an RBD diagnosis may require vPSG analysis. The diagnosis of RBD may also be supported by evaluation using various imaging techniques that are also useful in identifying synovial disorders, such as positron emission tomography (PET), single-photon emission computed tomography (SPECT), near-infrared photometry (NIR), magnetic resonance imaging (MRI), dopamine transporter imaging (DAT), or substantia nigra ultrasound. Standardized Multiple Systemic Atrophy Assessment Scale (MSAS) UMSARS ) The UMSARS scale is a well-known measure that combines physician reports and reports submitted by patients / caregivers to assess disease progression in MSA patients. The UMSARS scale can be used in clinical settings to evaluate MSA patients for the purpose of monitoring disease progression and / or quantifying response to treatment. The UMSARS scale consists of four parts: Part One It assesses historical information relating to symptoms and activities of daily living during the last two weeks as reported by patients and caregivers (12 items) and is assessed on a scale from 0 = unaffected to 4 = unable to perform the activity (Note: Each item uses different reference descriptions depending on the question asked). Part Two It consists of a clinical examination of MSA indicators and major motor symptoms (14 items) and is assessed on a scale ranging from 0 = normal to 4 = marked / severe deterioration (Note: Each item uses different reference descriptions depending on the question asked). Part Three It includes an autonomic nervous system examination (4 items), separate measurements of systolic and diastolic blood pressure, heart rate and orthostatic symptoms (yes / no). Part Four The overall degree of disability (one item) is assessed on a scale ranging from 1 = completely independent to 5 = completely dependent and incapacitated / bedridden. The overall score on the scale UMSARS The UMSARS TS is calculated using scores from items in Parts 1 and 2. Scores for Part 1 range from 0 to 48, while Part 2 ranges from 0 to 56. A higher score indicates a greater degree of deterioration. An experienced neurologist can administer the UMSARS scale after a short training session. scale degree UMSARS Rate (mUMSARS) In this context, it consists of Part 1 of the UMSARS scale, such that the two response options, 0 and 1, are combined into one category when performing the analysis. scale degree UMSARS The summary The aUMSARS score can be derived from a subset of items from Parts 1 and 2 of the UMSARS scale that have been shown to be patient-centered and sensitive to monitoring disease progression in MSA. Abbreviated UMSARS scales can be developed to be patient-centered (patient-relevant) and sensitive to detecting change in patients diagnosed with probable, likely, clinically confirmed, or clinically probable MSA. The abbreviated UMSARS score is based on a subset of items from Parts 1 and 2 of the original UMSARS scale. For example, items to be included in the aUMSARS score can be identified by 1) identifying change-sensitive items based on regression rates and / or patient-centered items based on their correlation with quality of life (QoL) measures, and 2) incorporating them into an abbreviated version of the UMSARS scale; that is, by excluding items with low patient-centeredness and low power to detect change over time.For example, data used to develop aUMSARS can be obtained from the natural history study conducted by the European Multiple System Atrophy (MSA) Study Group and from the MSA-Ras trial. The sensitivity of a sub-item of the MSA Unified Assessment Scale to change can be assessed by calculating the sensitivity ratio to change using the mean slope of its progression divided by the standard deviation of that slope when modeling its progression over time using a mixed linear model. The patient-centeredness of the scale can be assessed based on the correlation of MSA Unified Assessment Scale items with quality-of-life measures. An example of this aUMSARS scale is given below. This particular aUMSARS scale includes the following 19 items from Parts 1 and 2 of the UMSARS scale: Part 1 swallowing P1 Q2 handwriting P1 Q3 getting dressed P1 Q5 personal hygiene P1 Q6 Walking P1 Q7 Erectile symptoms P1 Q9 urinary symptoms P1 Q10 bowel function P1 Q12 Part 2 facial expressions P2 Q1 eye movement disorder P2 Q3 motor tremor P2 Q5 Increased muscle strength P2 Q6 Rapid alternating hand movements P2 Q7 tapping fingers P2 Q8 slim legs P2 Q9 Heel-knee-calf test P2 Q10 Getting up from the chair P2 Q11 situation P2 Q12 walk P2 Q14 Specific incarnations The following illustrations describe the invention in more detail. In one embodiment, the invention provides an anti-alpha-synocline monoclonal antibody for use in the treatment of synoclonic disorders or prodromal synoclonic disorders, where the use involves the intravenous administration of an anti-alpha-synocline monoclonal antibody to a person under treatment who has or is at risk of developing a synoclonic disorder, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synocline monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synocline (Sequence ID: 10). In one embodiment, the invention provides an anti-alpha-synoclane monoclonal antibody for use in the treatment of synoclane disorders, where the use involves the intravenous administration of an anti-alpha-synoclane monoclonal antibody to a person under treatment who has or is at risk of developing a synoclane disorder, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synoclane monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synoclane (Sequence ID: 10). In one embodiment, the invention provides an anti-alpha-synocline monoclonal antibody for use in the treatment of prodromal synoclonic disorders, where the use involves the intravenous administration of an anti-alpha-synocline monoclonal antibody to a person under treatment who has or is at risk of developing a synoclonic disorder, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synocline monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synocline (Sequence ID: 10). In one embodiment, the invention provides an anti-alpha-synuclein monoclonal antibody for use in the treatment of MSA, where the use involves the intravenous administration of an anti-alpha-synuclein monoclonal antibody to a person under treatment suffering from MSA, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, such as between 4000 mg and 7000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). In one embodiment, the invention provides an anti-alpha-synuclein monoclonal antibody for use in the treatment of MSA, where the use involves the intravenous administration of an anti-alpha-synuclein monoclonal antibody to a person under treatment suffering from MSA, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, such as between 4000 mg and 7000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). In one embodiment, the invention provides an anti-alpha-synuclein monoclonal antibody for use in the treatment of early MSA, where the use involves the intravenous administration of an anti-alpha-synuclein monoclonal antibody to a patient undergoing treatment who has early clinical MSA, at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, such as between 4000 mg and 7000 mg, or such as between 1000 mg and 4500 mg, where the anti-alpha-synuclein monoclonal antibody is a full-length antibody that binds to an epitope located within amino acids 112-117 (Sequence ID: 9) (ILEDMP) of human alpha-synuclein (Sequence ID: 10). In certain formulations, the monoclonal antibody directed against alpha-synuclein has an estimated KD value for binding to the oligomeric form of alpha-synuclein of approximately 0.5 nanomolar. In further embodiment, the monoclonal antibody directed against alpha-synuclein has a KD value for binding to the monomeric form of alpha-synuclein of approximately 36 nanomolar. In further embodiment, the monoclonal antibody directed against alpha-synuclein has a KD value for binding to the monomeric form of alpha-synuclein of approximately 36 nanomolars, and an estimated KD value for binding to the oligomeric form of alpha-synuclein of approximately 0.5 nanomolars. In one incarnation, the correlation ratio of the oligomeric form compared to the monomeric form is enhanced by approximately 65 times. In further embodiment, the monoclonal antibody directed against alpha-synuclein has a human ½T half-life of approximately 25-35 days, such as approximately 4 weeks, or approximately 27-33 days, or 28-32 days, or 28-30 days, or 28 days, or 29 days, or 30 days. In further embodiment, the monoclonal antibody directed against alpha-synuclein has a KD value for binding to the monomeric form of alpha-synuclein of approximately 36 nanomolars, and an estimated KD value for binding to the oligomeric form of alpha-synuclein of 0.5 nanomolars, such that the monomeric-to-oligomeric binding ratio is enhanced by approximately 65 times. In further embodiment, the monoclonal antibody directed against alpha-synuclein has a Kd value for binding to the monomeric form of alpha-synuclein of about 36 nanomolars, and an estimated Kd value for binding to the oligomeric form of alpha-synuclein of 0.5 nanomolars, such that the monomeric-to-oligomeric binding ratio is enhanced by about 65 times, and the antibody has a half-life of about 28-30 days, such as 29 days. In further embodiment, the monoclonal antibody directed against alpha-synuclein includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 2 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes a heavy chain consisting of a variable domain. Serial ID number :7 A light series consisting of a variable range Serial ID number :8 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 33 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes a heavy chain consisting of a variable domain. Serial ID number :30 A light series consisting of a variable range Serial ID number :8 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes a variable domain of a heavy chain consisting of Serial ID number :31 A variable range for a light chain consisting of Serial ID number :8 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 35 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . In further embodiment, the monoclonal antibody directed against alpha-synuclein includes a heavy chain consisting of a variable domain. Serial ID number :32 A light series consisting of a variable range Serial ID number :8 . In further embodiment, the monoclonal antibody directed against alpha-synuclein is a full-length human antibody. In further embodiment, the monoclonal antibody directed against alpha-synuclein is a human IgG1 antibody. In further incarnation, the monoclonal antibody directed against alpha-synuclein is GM37. In an additional incarnation, the monoclonal antibody directed against alpha-synuclein is GM37 Variant 1. In an additional incarnation, the monoclonal antibody directed against alpha-synuclein is GM37 Variant 2. In an additional incarnation, the monoclonal antibody directed against alpha-synuclein is GM37 Variant 3. In further embodiment, the monoclonal antibody directed against alpha-synuclein also includes a fixed heavy chain domain as defined in Serial ID number :18 And a fixed range for the Kappa-type light chain as defined in Serial ID number :17 . In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given every 4 weeks or 28 days. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given once a month. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given at a dose greater than 700 mg and less than 7000 mg, such as between 900 mg and 5000 mg, such as between 4000 mg and 7000 mg, or such as between 1000 mg and 4500 mg, at intervals of 3-5 weeks. In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given at a dose of 750 mg, 2250 mg, 4500 mg, or 6300 mg. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given at a dose ranging from 1000 mg to 4500 mg, such as between 2000 mg and 4500 mg, such as between 4000 mg and 7000 mg, or between 3500 mg and 4500 mg. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given at a dose of 750 mg, 1050 mg, 1400 mg, 1750 mg, 2100 mg, 2450 mg, 2800 mg, 3150 mg, 3500 mg, 3850 mg, 4200 mg, 4550 mg, 4900 mg, 5250 mg, 5600 mg, 5950 mg, 6300 mg, or 6650 mg. In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given at a dose of 1050 mg, 2100 mg, 4200 mg, or 6300 mg. In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given at a dose of 4200 mg. In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given at a dose of 6300 mg. In one of the incarnations, the dose is a fixed dose. In an additional formulation, the monoclonal antibody directed against alpha-synuclein is given at a dose of 1050 mg, 2100 mg, 4200 mg, or 6300 mg every 28-30 days. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given at a dose of 4200 mg every 4 weeks or every 28-30 days, such as every 28 days, every 29 days, or every 30 days. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given by intravenous infusion over 30 minutes ±10 minutes. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given by intravenous infusion over 15 minutes ±5 minutes. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given by intravenous infusion at a rate of between 25 mg / min and 300 mg / min. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given by intravenous infusion at a rate between 30 mg / min and 150 mg / min, such as 35 mg / min, 70 mg / min, or 140 mg / min. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given by intravenous infusion at a rate between 60 mg / min and 300 mg / min, such as 70 mg / min, 140 mg / min, or 280 mg / min. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated steady-state mean concentration in the cerebrospinal fluid (CSF) of the antibody of not less than 0.5 nanomolar, such as not less than 1 nanomolar, or not less than 2 nanomolar, or not less than 3 nanomolar, or not less than 6 nanomolar, or not less than 12 nanomolar, or such as 18 nanomolar. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated steady-state mean concentration of said antibody in the cerebrospinal fluid (CSF) of no less than 3 nanomolar. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated steady-state mean concentration of said antibody in the cerebrospinal fluid (CSF) of no less than 6 nanomolar. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated steady-state mean concentration of said antibody in the cerebrospinal fluid (CSF) of no less than 12 nanomolar. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated steady-state mean concentration of said antibody in cerebrospinal fluid (CSF) of no less than 18 nanomolar. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomers in the cerebrospinal fluid (CSF) of at least 50%, such as at least 60%, 75%, 80%, 85%, 90%, 95%, or 99%. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in cerebrospinal fluid (CSF) of at least 85%. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in cerebrospinal fluid (CSF) of at least 90%. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in cerebrospinal fluid (CSF) of at least 95%. In an additional embodiment, the monoclonal antibody directed against alpha-synuclein is given in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in cerebrospinal fluid (CSF) of at least 97%. In further embodiment, the synopathy to be treated is selected from a list consisting of: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, purely autonomic nervous system failure, and multiple system atrophy (MSA). In an additional embodiment, the synocular pathology to be treated is chosen from: Parkinson's disease (PD), dementia with Lewy bodies (DLB), or multiple system atrophy (MSA). In further embodiment, the synocular pathology to be treated is multiple systemic atrophy (MSA) or an MSA subtype chosen from: probable MSA, likely MSA, type C MSA, type P MSA, clinically confirmed MSA, or clinically probable MSA. In further embodiment, the synopathy to be treated is selected from: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and autonomic nervous system failure and multiple system atrophy (MSA). Treatment involves administering the anti-alpha-synocline monoclonal antibody to the patient in sufficient quantity and frequency to achieve a steady-state cerebrospinal fluid (CSF) concentration of the antibody of at least 0.5 nanomolar, such as at least 1 nanomolar, or at least 2 nanomolar, or at least 3 nanomolar, or at least 6 nanomolar, or at least 12 nanomolar. In further embodiment, the synopathy to be treated is selected from: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and autonomic nervous system failure and multiple system atrophy (MSA). Treatment involves administering the anti-alpha-synocline monoclonal antibody to the patient in sufficient quantity and frequency to achieve a steady-state cerebrospinal fluid (CSF) concentration of the antibody of at least 3 nanomolar, such as at least 6 nanomolar, or at least 12 nanomolar. In further embodiment, the invention provides a method for treating selected synonucleopathies from: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and autonomic nervous system failure and multiple system atrophy (MSA), where treatment involves administering an anti-alpha-synuclein monoclonal antibody to the patient in a quantity and at a frequency sufficient to achieve an estimated target binding to alpha-synuclein oligomers in the cerebrospinal fluid (CSF) of at least 50%, such as at least 60%, 75%, 80%, 85%, 90%, or 95%. 97%, or at least 99%. In further embodiment, the invention provides a method for treating selected synonucleopathy from: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and autonomic nervous system failure and multiple system atrophy (MSA), whereby the treatment involves administering the anti-alpha-synuclein monoclonal antibody to the patient in a quantity and frequency sufficient to achieve an estimated target binding to alpha-synuclein oligomeric forms in the cerebrospinal fluid (CSF) of not less than 85%, such as not less than 90%, or not less than 95%, or not less than 97%. In further embodiment, the invention provides a method for treating selected synocular dystrophies from: Parkinson's disease (PD) (including idiopathic and hereditary forms of Parkinson's disease), Gaucher disease (GD), diffuse Lewy body disease (DLBD), dementia with Lewy bodies (DLB), Lewy body variant of Alzheimer's disease (LBV), combined Alzheimer's and Parkinson's disease, and purely autonomic nervous system failure or multiple system atrophy (MSA). In a further embodiment, the invention provides a method for treating selected synocular dystrophy from: Parkinson's disease (PD), dementia with Lewy bodies (DLB), or multiple system atrophy (MSA). In further embodiment, the invention provides a method for treating synovial dystrophy that is multiple systemic atrophy (MSA) as an MSA subtype selected from: probable MSA, likely MSA, type C MSA, type P MSA, clinically confirmed MSA, or clinically probable MSA. In an additional embodiment, the invention provides a monoclonal antibody against alpha-synuclein, to treat a patient undergoing treatment who has multiple system atrophy (MSA) of the Parkinsonian subtype (MSA-P) or cerebellar subtype (MSA-C). In a further embodiment, the invention provides a monoclonal antibody against alpha-synuclein, to treat a patient undergoing treatment who has multiple system atrophy (MSA), such that it can be identified by the appearance of motor and / or autonomic nervous system-related (erectile or urinary) symptoms of MSA within the last 5 years, such as the last 4 years, 3 years, 2 years, or within the last year. In a further embodiment, the invention provides a monoclonal antibody against alpha-synuclein, to treat a patient undergoing treatment suffering from multiple system atrophy (MSA), such that it can be identified by obtaining a score ≤ 16 on the first part of the UMSARS scale (after excluding item 11 relating to sexual function). In a further embodiment, the invention provides a monoclonal antibody against alpha-synuclein, to treat a patient undergoing treatment who suffers from multiple system atrophy (MSA), such that he can be identified by obtaining cognitive performance assessed by the Montreal Cognitive Assessment (MoCA) of a score ≥ 22. In another preferred incarnation, the patient undergoing treatment for multiple systemic atrophy (MSA) has MSA-C. In another preferred incarnation, the patient undergoing treatment for MSA has MSA-P. In yet another preferred incarnation, the patient undergoing treatment for MSA has clinically probable or likely MSA-C. In yet another preferred incarnation, the patient undergoing treatment for MSA has clinically probable or likely MSA-P. In another preferred incarnation, the person undergoing treatment for multiple systemic atrophy (MSA) has early-stage MSA. In another similar incarnation, the person undergoing treatment for MSA has early-stage MSA. In yet another similar incarnation, the person undergoing treatment for MSA has early-stage MSA. In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple system atrophy (MSA) receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein.In another similar incarnation, a person undergoing treatment for multiple systemic atrophy (MSA) receives a total UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, 15-25, or 20-25, or 10-20, or 15-20, or 10-15 at the first infusion of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). In another preferred embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) is diagnosed with MSA-C and receives a total UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15.In another similar embodiment, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein.In another similar incarnation, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 when starting treatment with an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug).In another similar incarnation, a person undergoing treatment for multiple systemic atrophy (MSA) has MSA-C and receives an overall UMSARS TS score of <40, such as <39, <38, <37, <36, <35, <34, <33, <32, <31, <30, 10-39, 15-39, 20-39, 25-39, 30-39, 35-39, 10-35, 15-35, 20-35, 25-35, 30-35, 10-30, 15-30, 20-30, 25-30, 10-25, or 15-25, or 20-25, or 10-20, or 15-20, or 10-15 at the first infusion of an antibody directed against alpha-synuclein, such as GM37v2 (Amlenetug). In one interpretation, the treatment for synovitis is to delay or slow the progression of the disease. In one embodiment, the treatment for synovial dysfunction is to delay or slow down clinical progression. In one embodiment, the amount of delay or slowing in disease progression or clinical progression is quantified by longitudinal changes compared to baseline in any of the relevant Unified Multiple Systemic Atrophy Rating Scale (UMSARS) scores described here or any relevant parts of such scales, such as Part I, Part II, Part III or Part IV, or the change compared to baseline in any combination of such parts of the UMSARS scale. In further embodiment, the degree of delay or slowing in disease progression or clinical progression is quantified by longitudinal changes compared to baseline in scores of the first and / or second part of the Unified Multiple Systemic Atrophy Rating Scale (UMSARS), in the first part of the Modified UMSARS Scale (mUMSARS), or in the abbreviated UMSARS Scale (aUMSARS). In further embodiment, the degree of delay or slowing in disease progression or clinical development is quantified by longitudinal changes compared to baseline in scores of Part I or Part II of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS). In further embodiment, the degree of delay or slowing in disease progression or clinical development is quantified by longitudinal changes compared to baseline in the scores of Part I and Part II of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS). In further embodiment, the degree of delay or slowing in disease progression or clinical progression is quantified by longitudinal changes compared to baseline in scores of the Unified Multiple Systemic Atrophy Rating Scale Part 1 (UMSARS), the Modified UMSARS Part 1 (mUMSARS), and / or the UMSARS Part 2. In further embodiment, the amount of delay or slowing in disease progression or clinical progression is quantified by longitudinal changes compared to baseline in UMSARS TS scores, and / or UMSARS Part I, and / or mUMSARS and / or UMSARS Part II. In further embodiment, the degree of delay or slowing in disease progression or clinical development is determined quantitatively by longitudinal changes compared to baseline in the abbreviated UMSARS scale score (aUMSARS). In further embodiment, the degree of delay or slowing in disease progression or clinical development is quantified by longitudinal changes compared to baseline in the modified UMSARS scale score (mUMSARS). In further embodiment, the degree of delay or slowing in disease progression or clinical development is determined quantitatively by longitudinal changes compared to baseline in the overall score of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS TS). In a further embodiment, the amount of delay or slowing in disease progression or clinical development is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI). In further embodiment, the degree of delay or slowing in the progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the bridge. In further embodiment, the degree of delay or slowing in the progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum white matter. In further embodiment, the degree of delay or slowing in the progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum gray matter. In further embodiment, the degree of delay or slowing in the clinical progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the bridge. In further embodiment, the degree of delay or slowing in the clinical progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum white matter. In further embodiment, the degree of delay or slowing in the clinical progression of MSA disease is determined quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum gray matter. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately at least 10%, for example, at least 15%, or at least 20%, or at least 30%, or at least 35%, or 10-35%, or 15-35%, or 19-35%, or 20-35%, or 25-35%, or 30-35%, or 10-30%, or 15-30%, or 19-30%, or 20-30%, or 25-30%, or 10-25%, or 15-25%, or 19-25%, or 20-25%, or 10-20%, or 15-20%, or 19-20%, or 10-15%, of The amount of clinical progression slowdown in MSA measured by the total UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is at least 19% of the amount of clinical progression slowdown in MSA measured by the total UMSARS score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 10-35%, 15-35%, 19-35%, 20-35%, 25-35%, 30-35%, 10-30%, 15-30%, 19-30%, 20-30%, 25-30%, 10-25%, 15-25%, 19-25%, 20-25%, 10-20%, 15-20%, 19-20%, or 10-15% of the amount of clinical progression slowdown in MSA measured by the overall UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately 19% of the amount of clinical progression slowing in MSA as measured by the total score of the UMSARS scale. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately at least 10%, e.g., at least 15%, at least 20%, at least 30%, at least 35%, 10-35%, 15-35%, 20-35%, 22-35%, 25-35%, 30-35%, 10-30%, 15-30%, 20-30%, 22-30%, 25-30%, 10-25%, 15-25%, 20-25%, 22-25%, 10-20%, 15-20%, or 10-15%, of the amount of slowing of clinical progression in MSA measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is at least 22% of the amount of clinical progression slowing in MSA measured by the UMSARS Part 1 score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 10-35%, or 15-35%, or 20-35%, or 22-35%, or 25-35%, or 30-35%, or 10-30%, or 15-30%, or 20-30%, or 22-30%, or 25-30%, or 10-25%, or 15-25%, or 20-25%, or 22-25%, or 10-20%, or 15-20%, or 10-15% of the amount of clinical progression slowdown in MSA measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately 22% of the amount of slowing of clinical progression in MSA as measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately at least 10%, for example, at least 15%, at least 20%, at least 30%, at least 35%, 10-35%, 15-35%, 17-35%, 20-35%, 25-35%, 30-35%, 10-30%, 15-30%, 17-30%, 20-30%, 25-30%, 10-25%, 15-25%, 17-25%, 20-25%, 10-20%, 15-20%, 17-20%, or 10-15% of The amount of clinical progression slowdown in MSA measured by the UMSARS Part II score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is at least 17% of the amount of clinical progression slowdown in MSA measured by the UMSARS Part II score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 10-35%, or 15-35%, or 17-35%, or 20-35%, or 25-35%, or 30-35%, or 10-30%, or 15-30%, or 17-30%, or 20-30%, or 25-30%, or 10-25%, or 15-25%, or 17-25%, or 20-25%, or 10-20%, or 15-20%, or 17-20%, or 10-15% of the amount of clinical progression slowdown in MSA measured by the UMSARS Part II score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately 17% of the amount of slowing of clinical progression in MSA as measured by the UMSARS Part II score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 10%, e.g., at least 15%, at least 20%, at least 30%, at least 35%, 10-35%, 15-35%, 20-35%, 25-35%, 27-35%, 30-35%, 10-30%, 15-30%, 20-30%, 25-30%, 27-30%, 10-25%, 15-25%, 20-25%, 10-20%, 15-20%, or 10-15%, of the clinical progression slowdown in MSA as measured by the UMSARS score. The average. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is at least 27% of the amount of clinical progression slowing in MSA as measured by the modified UMSARS score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 10-35%, 15-35%, 20-35%, 25-35%, 27-35%, 30-35%, 10-30%, 15-30%, 20-30%, 25-30%, 27-30%, 10-25%, 15-25%, 20-25%, 10-20%, 15-20%, or 10-15% of the amount of clinical progression slowdown in MSA measured by the modified UMSARS scale. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately 27% of the clinical progression slowdown in MSA as measured by the modified UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately at least 30%, for example, at least 40%, or at least 50%, or at least 60%, or at least 70%, or at least 80%, or at least 90%, or at least 95%, or 30-99%, or 40-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 60–80%, or 70–80%, or 30–70%, or 40–70%, or 50–70%, or 60–70%, or 30–60%, or 40–60%, or 50–60%, or 30–50%, or 40–50%, or 30–40% of the clinical progression slowdown in MSA-C as measured by the modified UMSARS score. In further embodiment, treatment with GM37v2 (Amlenetug) administered every 4 weeks or once a month results in at least 50% of the clinical progression slowdown in MSA-C as measured by the modified UMSARS score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 30-99%, or 40-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, 50-60%, 30-50%, 40-50%, or 30-40% of the clinical progression slowdown in MSA-C as measured by the modified UMSARS score. In further embodiment, treatment with GM37v2 (Amlenetug) administered every 4 weeks or once a month results in approximately 50% of the clinical progression slowdown in MSA-C as measured by the modified UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately at least 30%, for example, at least 40%, or at least 50%, or at least 60%, or at least 70%, or at least 80%, or at least 90%, or at least 95%, or 30-99%, or 40-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 50-60%, or 30-50%, or 40-50%, or 30-40% of the clinical progression slowdown in MSA-C as measured by the UMSARS total score. In further embodiment, treatment with GM37v2 (Amlenetug) administered every 4 weeks or once a month results in at least 50% of the clinical progression slowdown in MSA-C as measured by the UMSARS total score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is at least 50% of the amount of clinical progression slowing in MSA-C as measured by the overall UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 30-99%, or 40-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 50-60%, or 30-50%, or 40-50%, or 30-40% of the clinical progression slowdown in MSA-C as measured by the total UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment given every 4 weeks or once a month is approximately 50% of the clinical progression slowdown in MSA-C as measured by the total UMSARS score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately at least 30%, for example, at least 40%, or at least 50%, or at least 57%, or at least 60%, or at least 70%, or at least 80%, or at least 90%, or at least 95%, or 30-99%, or 40-99%, or 50-99%, or 57-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 57-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 57-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 50-70%, or 57-70%, or 60-70%, or 30-60%, or 40-60%, or 50-60%, or 57-60%, or 30-50%, or 40-50%, or 30-40% of the amount of clinical progression slowdown in MSA-C measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is at least 57% of the amount of clinical progression slowdown in MSA-C as measured by the UMSARS Part 1 score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 30-99%, or 40-99%, or 50-99%, or 57-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 50-90%, or 57-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 50-80%, or 57-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 50-70%, or 57-70%, or 60-70%, or 30-60%, or 40-60%, or 50-60%, or 57-60%, or 30-50%, or 40-50%, or 30-40% of the clinical progression delay in MSA-C as measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment administered every 4 weeks or once a month is approximately 57% of the clinical progression delay in MSA-C as measured by the UMSARS Part 1 score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately at least 30%, for example, at least 40%, or at least 41%, or at least 50%, or at least 60%, or at least 70%, or at least 80%, or at least 90%, or at least 95%, or 30-99%, or 40-99%, or 41-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 41-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 41-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 41-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 41-60%, or 50-60%, or 30-50%, or 40-50%, or 41-50%, or 30-40% of the amount of clinical progression slowdown in MSA-C measured by the UMSARS Part II score. In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is at least 41% of the clinical progression slowdown in MSA-C as measured by the UMSARS Part II score.In further embodiment, the effect of GM37v2 (Amlenetug) therapy given every 4 weeks or once a month is approximately 30-99%, or 40-99%, or 41-99%, or 50-99%, or 60-99%, or 70-99%, or 80-99%, or 90-99%, or 30-90%, or 40-90%, or 41-90%, or 50-90%, or 60-90%, or 70-90%, or 80-90%, or 30-80%, or 40-80%, or 41-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 41-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 41-60%, or 50-60%, or 30-50%, or 40-50%, or 41-50%, or 30-40% of the clinical progression delay in MSA-C as measured by the UMSARS Part II score. In further embodiment, the effect of GM37v2 (Amlenetug) treatment administered every 4 weeks or once a month is approximately 41% of the clinical progression delay in MSA-C as measured by the UMSARS Part II score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C cases, is a slowing of the localized volumetric decrease in the bridge by approximately 0.8–1.5%, for example, 1.0–1.5%, 1.2–1.5%, 0.8–1.2%, 1–1.2%, or 0.8–1.0%, i.e., with a smaller volumetric decrease. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C cases, is a slowing of the localized volumetric decrease in the bridge by approximately 1.2%, i.e., with a smaller volumetric decrease. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar white matter by approximately 2.5–5%, 3–5%, 3.5–5%, 4–5%, 2.5–4%, 3–4%, 3.5–4%, or 2.5–3%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar white matter by approximately 3.8%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar gray matter by approximately 0.2–0.6%, for example, 0.3–0.6%, 0.4–0.6%, 0.5–0.6%, 0.3–0.5%, 0.4–0.5%, or 0.3–0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar gray matter by approximately 0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C cases, is a slowing of the localized volumetric decrease in the bridge by at least approximately 0.8–1.5%, for example, 1.0–1.5%, 1.2–1.5%, 0.8–1.2%, 1–1.2%, or 0.8–1.0%, i.e., with a smaller volumetric decrease. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C cases, is a slowing of the localized volumetric decrease in the bridge by at least approximately 1.2%, i.e., with a smaller volumetric decrease. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar white matter by at least 2.5–5%, 3–5%, 3.5–5%, 4–5%, 2.5–4%, 3–4%, 3.5–4%, or 2.5–3%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar white matter by at least 3.8%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar gray matter by at least approximately 0.2–0.6%, for example, 0.3–0.6%, 0.4–0.6%, 0.5–0.6%, 0.3–0.5%, 0.4–0.5%, or 0.3–0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA-C, is a slowing of the local volume reduction in cerebellar gray matter by at least approximately 0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 30%, for example, at least 40%, 42%, 50%, 60%, 70%, 80%, 90%, 95%, or 30-99%, 40-99%, 42-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 40-90%, 42-90%, 50-90%, 60-90%, 70-90%, 80-90%, or 30-80%, or 40-80%, or 42-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 42-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 42-60%, or 50-60%, or 30-50%, or 40-50%, or 42-50%, or 30-40%, in clinical disease progression in early MSA patients when assessed using the modified UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 42% in clinical disease progression in early MSA patients when assessed using the modified UMSARS scale.In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of approximately 30-99%, 40-99%, 42-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 40-90%, 42-90%, 50-90%, 60-90%, 70-90%, 80-90%, 30-80%, 40-80%, 42-80%, 50-80%, 60-80%, 70-80%, 30-70%, or 40-70%, or 42-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 42-60%, or 50-60%, or 30-50%, or 40-50%, or 42-50%, or 30-40% in clinical disease progression in patients with early-onset MSA when assessed using the modified UMSARS scale. Furthermore, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month is a slowing of approximately 42% in clinical disease progression in patients with early-onset MSA when assessed using the modified UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks is a slowing of at least approximately 30%, for example, at least 40%, 50%, 60%, 70%, 80%, 90%, 95%, 30-99%, 37-99%, 40-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 37-90%, 40-90%, 50-90%, 60-90%, 70-90%, 80-90%, 30-80%, or 37-80%, or 40-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 37-70%, or 40-70%, or 50-70%, or 60-70%, or 30-60%, or 37-60%, or 40-60%, or 50-60%, or 30-50%, or 37-50%, or 40-50%, or 37-40%, or 30-40%, in clinical disease progression in early MSA patients when assessed using the UMSARS total score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 37% in clinical disease progression in early MSA patients when assessed using the overall score of the UMSARS scale.In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of approximately 30-99%, 37-99%, 40-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 37-90%, 40-90%, 50-90%, 60-90%, 70-90%, 80-90%, 30-80%, 37-80%, 40-80%, 50-80%, 60-80%, 70-80%, 30-70%, or 37-70%, or 40-70%, or 50-70%, or 60-70%, or 30-60%, or 37-60%, or 40-60%, or 50-60%, or 30-50%, or 37-50%, or 40-50%, or 37-40%, or 30-40% in clinical disease progression in patients with early-onset MSA when assessed using the UMSARS total score. Furthermore, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks is a slowing of approximately 37% in clinical disease progression in patients with early-onset MSA when assessed using the UMSARS total score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 30%, for example, at least 40%, 42%, 50%, 60%, 70%, 80%, 90%, 95%, or 30-99%, 40-99%, 42-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 40-90%, 42-90%, 50-90%, 60-90%, 70-90%, 80-90%, or 30-80%, or 40-80%, or 42-80%, or 50-80%, or 60-80%, or 70-80%, or 30-70%, or 40-70%, or 42-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 42-60%, or 50-60%, or 30-50%, or 40-50%, or 42-50%, or 30-40%, in clinical disease progression in early MSA patients when assessed using the first part of the UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 42% in clinical disease progression in early MSA patients when assessed using the first part of the UMSARS scale.In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of approximately 30-99%, 40-99%, 42-99%, 50-99%, 60-99%, 70-99%, 80-99%, 90-99%, 30-90%, 40-90%, 42-90%, 50-90%, 60-90%, 70-90%, 80-90%, 30-80%, 40-80%, 42-80%, 50-80%, 60-80%, 70-80%, 30-70%, or 40-70%, or 42-70%, or 50-70%, or 60-70%, or 30-60%, or 40-60%, or 42-60%, or 50-60%, or 30-50%, or 40-50%, or 42-50%, or 30-40% in clinical disease progression in patients with early-onset MSA when assessed using the first part of the UMSARS scale. Furthermore, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month is a slowing of approximately 42% in clinical disease progression in patients with early-onset MSA when assessed using the first part of the UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 10%, for example, at least 15%, 20%, 30%, 35%, 40%, or 50%, or 10-50%, 15-50%, 20-50%, 25-50%, 30-50%, 35-50%, 40-50%, 45-50%, 10-45%, 15-45%, 20-45%, 25-45%, 30-45%, 35-45%, 40-45%, 10-40%, or 15-40%. 20-40%, or 25-40%, or 30-40%, or 35-40%, or 10-35%, or 15-35%, or 20-35%, or 25-35%, or 30-35%, or 10-30%, or 15-30%, or 20-30%, or 25-30%, or 10-25%, or 15-25%, or 20-25%, or 10-20%, or 15-20%, or 10-15%, in clinical disease progression in early MSA patients when assessed using the second part of the UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of at least approximately 30% in clinical disease progression in early MSA patients when assessed using the second part of the UMSARS scale.In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month is a slowing of approximately 10-50%, or 15-50%, or 20-50%, or 25-50%, or 30-50%, or 35-50%, or 40-50%, or 45-50%, or 10-45%, or 15-45%, or 20-45%, or 25-45%, or 30-45%, or 35-45%, or 40-45%, or 10-40%, or 15-40%, or 20-40%, or 25-40%, or 30-40%, or 35-40%, or 10-35%, or 15-35%, or 20-35%, or 25-35%, or 30-35%, or 10-30%, or 15-30%, or 20-30%, or 25-30%, or 10-25%, or 15-25%, or 20-25%, or 10-20%, or 15-20%, or 10-15% in clinical disease progression in patients with early-onset MSA when assessed using the second part of the UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month is an approximately 30% slowdown in clinical disease progression in patients with early-onset MSA when assessed using the second part of the UMSARS scale. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of localized bridge volume loss by approximately 1.8–3.0%, 2–2.8%, 2.2–2.6%, or 2.3–2.5%, respectively, with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of localized bridge volume loss by approximately 2.4%, with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of the local volume reduction in cerebellar white matter by approximately 3–5%, 3.5–4.5%, 4–5%, or 4–4.5%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of the local volume reduction in cerebellar white matter by approximately 4.2%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of the local volume reduction in cerebellar gray matter by approximately 0.2–0.6%, for example, 0.3–0.6%, 0.4–0.6%, 0.5–0.6%, 0.3–0.5%, 0.4–0.5%, or 0.3–0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of the local volume reduction in cerebellar gray matter by approximately 0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of localized bridge volume loss by at least 2.4%, i.e., with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of localized bridge volume loss by approximately 1.8–3.0%, 2–2.8%, 2.2–2.6%, or 2.3–2.5%, i.e., with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of the local volume reduction in cerebellar white matter by at least 4.2%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of the local volume reduction in cerebellar white matter by approximately 3–5%, 3.5–4.5%, 4–5%, or 4–4.5%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of the local volume reduction in cerebellar gray matter by at least approximately 0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of the local volume reduction in cerebellar gray matter by at least approximately 0.2–0.6%, e.g., 0.3–0.6%, 0.4–0.6%, 0.5–0.6%, 0.3–0.5%, 0.4–0.5%, or 0.3–0.4%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in cases of MSA is a slowing of deterioration as measured by the fourth part of the UMSARS scale - the overall disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in early MSA cases is a slowing of deterioration as measured by the fourth part of the UMSARS scale - the overall disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in cases of MSA-C is a slowing of deterioration as measured by the fourth part of the UMSARS scale - the overall disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA cases, is a slowing of deterioration as measured by Part IV of the UMSARS scale – the overall disability score – by approximately 0.1–0.3, 0.2–0.3, or 0.1–0.2, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA cases, is a slowing of deterioration as measured by Part IV of the UMSARS scale – the overall disability score – by approximately 0.2, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of deterioration as measured by Part IV of the UMSARS scale – the overall disability score – by approximately 0.6–1.0, 0.7–1.0, 0.8–1.0, 0.6–0.9, 0.7–0.9, 0.6–0.8, or 0.7–0.8, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of deterioration as measured by Part IV of the UMSARS scale – the overall disability score – by approximately 0.8, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of deterioration as measured by the UMSARS Part IV - Total Disability Score by at least approximately 0.8, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a slowing of deterioration as measured by the UMSARS Part IV - Total Disability Score by approximately 0.6-1.0, 0.7-1.0, 0.8-1.0, 0.6-0.9, 0.7-0.9, 0.6-0.8, or 0.7-0.8, i.e., a decrease in the disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a slowing of progression as measured by the Clinical Impression Scale – Disease Severity. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of early MSA, is a slowing of progression as measured by the Clinical Impression Scale – Disease Severity. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in cases of MSA-C is a slowing of deterioration as measured by the overall clinical impression scale - disease severity. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in MSA is a slowing of deterioration as measured by the Clinical Impression Severity Scale by at least 0.2, i.e., a reduction in disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in MSA is a slowing of deterioration as measured by the Clinical Impression Severity Scale by approximately 0.1-0.3, 0.2-0.3, or 0.1-0.2, i.e., a reduction in disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in MSA is a slowing of deterioration as measured by the Clinical Impression Severity Scale by approximately 0.2, i.e., a reduction in disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of progression as measured by the Clinical Impression Severity Scale (CISS) by at least 0.5, i.e., a reduction in disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of progression as measured by the Clinical Impression Severity Scale (CISS) by approximately 0.3–0.7, 0.3–0.6, 0.3–0.5, 0.4–0.7, 0.4–0.6, 0.5–0.7, or 0.5–0.6, i.e., a reduction in disability score. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA cases, is a slowing of deterioration as measured by the overall clinical impression scale - disease severity by about 0.5, i.e., with a decrease in the degree of disability. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in MSA is a slowing of localized bridge volume loss by at least approximately 1.9%, i.e., with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in MSA is a slowing of localized bridge volume loss by approximately 1–3%, 1.5–3%, 1.9–3%, 2–3%, 1–2.5%, 1–2%, 1.5–2%, 1–1.9%, or 1.9–2.5%, i.e., with less volume loss. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), given every 4 weeks or once a month in cases of MSA, is a slowing of the local volumetric decrease in the bridge by approximately 1.9%, i.e., with less volumetric decrease. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in cases of MSA is a slowing of the local volume reduction in the cerebellar white matter by at least about 3.3%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) given every 4 weeks or once a month in cases of MSA is a slowing of the local volume reduction in the cerebellar white matter by approximately 2-5%, or 2.5-5%, or 3-5%, or 3.3-5%, or 2-4%, or 2.5-4%, or 3-4%, or 3.3-4%, or 2-3.5%, or 2.5-3.5%, or 3-3.5%, or 2-3.3%, or 2.5-3.3%, or 3-3.3%, i.e. with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), given every 4 weeks or once a month in cases of MSA, is a slowing of the local volume reduction in the cerebellar white matter by about 3.3%, i.e., with less volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a slowing of the local volume reduction in cerebellar gray matter by at least approximately 1.5%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a slowing of the local volume reduction in cerebellar gray matter by approximately 1–3%, 1–2.5%, 1–2%, 1–1.5%, 1.5–3%, 1.5–2.5%, or 1.5–2%, i.e., with a smaller volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), given every 4 weeks or once a month in cases of MSA, is a slowing of the local volume reduction in the gray matter of the cerebellum by about 1.5%, i.e., with less volume reduction. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a greater reduction in the level of nerve fiber light chains in the cerebrospinal fluid (CSF). In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a reduction in the level of nerve fiber light chains in the CSF by at least approximately 16.3%. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a reduction in the level of nerve fiber light chains in the cerebrospinal fluid (CSF) by approximately 10-25%, 10-20%, 10-16.3%, 10-15%, 15-25%, 15-20%, 15-16.3%, 16.3-25%, or 16.3-20%. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), administered every 4 weeks or once a month in cases of MSA, is a reduction in the level of nerve fiber light chains in the CSF by approximately 16.3%. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a reduction in the level of nerve fiber light chains in the cerebrospinal fluid (CSF) by at least approximately 14.4%. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug) administered every 4 weeks or once a month in early MSA is a reduction in the level of nerve fiber light chains in the CSF by approximately 5-25%, 10-25%, 14.4-25%, 15-25%, 20-25%, 5-20%, 10-20%, 14.4-20%, 15-20%, 5-15%, 10-15%, or 5-10%. In further embodiment, the therapeutic effect of GM37v2 (Amlenetug), given every 4 weeks or once a month in cases of early MSA, is a decrease in the level of light chain nerve fibers in the cerebrospinal fluid (CSF) by approximately 14.4%. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA, is a slowing of deterioration as measured by the single item "Speech" in Part 1 of the UMSARS scale. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA, is a slowing of deterioration as measured by the single item "Speech" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.4. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item “Speech” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2-0.6, or 0.3-0.6, or 0.4-0.6, or 0.5-0.6, or 0.2-0.5, or 0.3-0.5, or 0.4-0.5, or 0.2-0.4, or 0.3-0.4, or 0.2-0.3.In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration as measured by the single item “Speech” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.4. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA-C disease, is to slow deterioration as measured by the single item “Speech” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “Speech” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item "Speech" in Part I of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.8. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item "Speech" in Part I of the UMSARS scale, with a decrease in the deterioration score of approximately 0.6-1.0, 0.7-1.0, 0.8-1.0, 0.6-0.9, 0.7-0.9, 0.6-0.8, or 0.7-0.8. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow the deterioration as measured by the single item “Speech” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.8. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA, is a slowing of deterioration as measured by the single item "Cutting Food / Using Cutlery" in Part 1 of the UMSARS scale. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA, is a slowing of deterioration as measured by the single item "Cutting Food / Using Cutlery" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration according to the single item measure of "cutting food / using cutlery" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2-0.4, 0.3-0.4, or 0.2-0.3.In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration according to the single item measure of "cutting food / using cutlery" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA-C disease, is to slow deterioration as measured by the single item “cutting food / use of cutlery” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “cutting food / using cutlery” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item “cutting food / using cutlery” in the first part of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.7. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item "Cutting Food / Using Cutlery" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of approximately 0.5-0.9, 0.6-0.9, 0.7-0.9, 0.5-0.8, 0.6-0.8, 0.7-0.8, 0.5-0.7, or 0.6-0.7. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item "Cutting Food / Using Cutlery" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of approximately 0.7. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "Personal Hygiene" in Part 1 of the UMSARS scale. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "Personal Hygiene" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration according to the single item measure of "personal hygiene" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.1-0.3, 0.2-0.3, or 0.1-0.2.In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration according to the single item measure of "personal hygiene" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA-C disease, is to slow deterioration according to the single item measure of "personal hygiene" in the first part of the UMSARS scale. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of deterioration as measured by the single item "Personal Hygiene" in Part 1 of the UMSARS scale. In another manifestation, the effect of treatment with GM37v2 (Amlenetug), administered every 4 weeks or once a month in early MSA, is a slowing of deterioration as measured by the single item "Personal Hygiene" in Part 1 of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.6. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration according to the single item measure of "personal hygiene" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.4-0.8, or 0.5-0.8, or 0.6-0.8, or 0.7-0.8, or 0.4-0.7, or 0.5-0.7, or 0.6-0.7, or 0.4-0.6, or 0.5-0.6, or 0.4-0.5.In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow the deterioration according to the single item measure of "personal hygiene" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.6. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration as measured by the single item “walking” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "walking" in the first part of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "walking" in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.1-0.3, 0.2-0.3, or 0.1-0.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration as measured by the single item “walking” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA-C disease, is to slow deterioration as measured by the single item “walking” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “walking” in the first part of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow the deterioration as measured by the single item “walking” in the first part of the UMSARS scale, with a decrease in the deterioration score of at least about 0.4. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item “walking” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2-0.6, or 0.3-0.6, or 0.4-0.6, or 0.5-0.6, or 0.2-0.5, or 0.3-0.5, or 0.4-0.5, or 0.2-0.4, or 0.3-0.4, or 0.2-0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow the deterioration as measured by the single item “walking” in the first part of the UMSARS scale, with a decrease in the deterioration score of approximately 0.4. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "getting up from the chair" in Part II of the UMSARS scale, with a decrease in the deterioration score of at least approximately 0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is a slowing of deterioration as measured by the single item "getting up from the chair" in Part II of the UMSARS scale, with a decrease in the deterioration score of approximately 0.2-0.4, 0.3-0.4, or 0.2-0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA disease, is to slow the deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the deterioration score of approximately 0.3. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in MSA-C disease, is to slow deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the deterioration score of at least approximately 1.2. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is a slowing of deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the deterioration score of approximately 1.0-1.4, or 1.1-1.4, or 1.2-1.4, or 1.3-1.4, or 1.0-1.3, or 1.1-1.3, or 1.2-1.3, or 1.0-1.2, or 1.1-1.2, or 1.0-1.1. In another embodiment, the effect of treatment with GM37v2 (Amlenetug), given every 4 weeks or once a month in early MSA disease, is to slow deterioration as measured by the single item “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the deterioration score of approximately 1.2. In another embodiment, the treatment for synovitis consists of delaying or slowing the progression of the disease by at least 5%, such as at least 10%, or at least 15%, or at least 20%, or at least 25%, or at least 30%, or at least 35%, or at least 40%, or at least 45%, or at least 50%, or at least 55%, or at least 60%, or at least 65%, or at least 70%, or at least 75%, or at least 80%, or at least 85%, or at least 90%. In another embodiment, the treatment for synovitis consists of delaying disease progression by at least 25%, such as at least 30%, or at least 35%, or at least 40%. In another embodiment, the therapeutic effect in synovial dyspathy is observed after the administration of at least 10 doses of GM37v2 (Amlenetug), such as at least 11 doses, or at least 12 doses, or at least 13 doses, or at least 14 doses, or at least 15 doses, or at least 16 doses, or at least 17 doses, or at least 18 doses, or at least 19 doses, or at least 20 doses. In another embodiment, the effect of treatment in synovial dysfunction is observed after treatment with GM37v2 (Amlenetug) for at least 24 weeks, such as at least 48 weeks, at least 72 weeks, or at least 96 weeks. In another embodiment, the therapeutic effect in synovial dysfunction is observed after treatment with GM37v2 (Amlenetug) for at least 44 weeks or at least 48 weeks. In another embodiment, the effect of treating synovial dysfunction is observed after administering at least 10 doses of GM37v2 (Amlenetug), such as at least 11 doses, or at least 12 doses. In one of these incarnations, the person undergoing treatment for MSA has MSA-C. In another of these incarnations, the person undergoing treatment for MSA has MSA-P. In another of these incarnations, the person undergoing treatment for MSA has possible or probable MSA-C. In yet another of these incarnations, the person undergoing treatment for MSA has possible or probable MSA-P. In another embodiment, the delay in disease progression is quantified by longitudinal changes compared to baseline in blood concentrations of nerve fiber light chain (NfL). In another embodiment, the delay or slowing of disease progression in MSA is measured quantitatively by longitudinal changes compared to baseline in blood concentrations of neurofilament light chain (NfL). In another embodiment, disease progression delay is quantified by longitudinal changes compared to baseline in one or more of the following indicators: Schwab and England Activities of Daily Living (SE-ADL) score; or change compared to baseline in the Clinical General Impression Scale - Severity of Illness (CGI-S) score; or change compared to baseline in the Patient General Impression Scale - Severity of Illness (PGI-S) score; or change compared to baseline in the Assessor General Impression Scale - Severity of Illness (OGI-S) score; or change compared to baseline in the Compass Select Change score; or change compared to baseline in the UMSARS Part IV score; or change compared to baseline in the speech, swallowing, falling, and walking items, as assessed using the UMSARS Part I item scores; or change compared to baseline in the rate, causes, and consequences of falls, as assessed using fall logs or diaries; or change compared to baseline in the EuroQol 5D-5L five-dimensional and five-level scale; or change compared to baselineIn brain volume, using volumetric magnetic resonance imaging (vMRI); or change compared to baseline in tissue integrity, as measured using diffusion tensor magnetic resonance imaging (DTI); or change compared to baseline in blood concentrations of neural filament light chains (NfL); or change compared to baseline in heart rate, blood pressure, and postural symptoms, as assessed in the third part of the UMSARS scale; or change compared to baseline in gait parameters or fall rate, as measured by wearable digital sensors capable of tracking relevant gait parameters and / or recording falls; or change compared to baseline in cerebral blood flow, using magnetic resonance imaging with arterial spindle labeling (ASL); or change compared to baseline in total tau protein and NfL chain concentrations in cerebrospinal fluid (CSF); or change compared to baseline in the concentration of pathological alpha-synuclein species in CSF. In another embodiment, a person undergoing treatment who is at risk of developing a synopathy or has precursor synopathy can be identified by exhibiting one or more clinical signs of precursor synopathies selected from a group that includes: REM sleep behavior disorder (RBD) such as isolated RBD (iRBD), olfactory disorder such as hyposmia, abnormal cognitive performance on neuropsychological tests, mild motor dysfunction or abnormal motor performance assessed by objective tests, color vision disorder, autonomic nervous system disorders (such as constipation, urinary symptoms, erectile dysfunction, and orthostatic hypotension), reduced black striatal dopaminergic binding in the pituitary and striatum (abnormal DAT-SPECT), seborrheic dermatitis, and a genotype associated with an increased risk of phenotypic transformation such as mutations in the glucocerebrosidase enzyme (encoded by the GBA gene). In another embodiment, a person undergoing treatment who is at risk of developing synopathy or has prodromal synopathy can be identified by exhibiting RBD such as isolated RBD (iRBD), and at least one additional clinical sign of prodromal synopathies, such as hyposmia and / or abnormal DAT-SPECT. In another embodiment, the treatment for prodromal syncytial syndrome consists of delaying the onset of the disease. In another embodiment, the treatment for prodromal syncytial virus disease consists of delaying the onset or time of diagnosis by at least 5%, such as at least 10%, or at least 15%, or at least 20%, or at least 25%, or at least 30%, or at least 35%, or at least 40%, or at least 45%, or at least 50%, or at least 55%, or at least 60%, or at least 65%, or at least 70%, or at least 75%, or at least 80%, or at least 85%, or at least 90%. In another embodiment, the treatment for prodromal syncytia consists of delaying the onset of the disease or the time of diagnosis by at least 6 months, such as at least 8 months, or at least 10 months, or at least 12 months, or at least 14 months, or at least 16 months, or at least 18 months, or at least 20 months, or at least 22 months, or at least 24 months, or at least 2 years, or at least 3 years, or at least 4 years, or at least 5 years. In another embodiment, the invention provides a method for treating prodromal synuclein disease whereby the treatment involves administering an anti-alpha-synuclein monoclonal antibody in sufficient quantity and frequency to achieve a steady-state antibody concentration in the cerebrospinal fluid (CSF) of not less than 0.5 nanomolar, such as at least 1 nanomolar, or at least 2 nanomolar, or at least 3 nanomolar, or at least 6 nanomolar, or at least 12 nanomolar. In another embodiment, the invention provides a method for treating prodromal synonucleopathy, whereby the treatment involves administering an anti-alpha-synonuclein monoclonal antibody in sufficient quantity and frequency to achieve a steady-state antibody concentration in the cerebrospinal fluid (CSF) of at least 3 nanomolar, such as at least 6 nanomolar, or at least 12 nanomolar. In another embodiment, the invention provides a method for treating prodromal synuclein disease whereby the treatment involves administering an anti-alpha-synuclein monoclonal antibody in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in the cerebrospinal fluid (CSF) of not less than 50%, such as at least 60%, or at least 75%, or at least 80%, or at least 85%, or at least 90%, or at least 95%, or at least 99%. In another embodiment, the invention provides a method for treating prodromal synuclein disease whereby the treatment involves administering an anti-alpha-synuclein monoclonal antibody in sufficient quantity and frequency to achieve an estimated target binding to alpha-synuclein oligomeric forms in the cerebrospinal fluid (CSF) of not less than 85%, such as at least 90%, or at least 95%. In one aspect, this invention also provides for the use of a liquid pharmaceutical formulation containing a full-length IgG1 anti-alpha-synuclein monoclonal antibody at a concentration of 25-225 mg / ml, where the said antibody includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number : 6 ; And where the formulation also includes a histidine buffer, a pharmaceutically acceptable tensile agent, and a pharmaceutically acceptable surfactant, and where the pH of the formulation is between 5.5 and 6.5, this liquid pharmaceutical formulation is suitable for use in administering the anti-alpha-synoclane monoclonal antibody in any of the therapies, modalities, or uses described in aspects of this application, its incarnations, or its protective elements. In one embodiment, the monoclonal antibody in the liquid pharmaceutical formulation includes a variable heavy chain domain consisting of Serial ID number : 31 A variable range of the light chain consists of Serial ID number : 8 . In one incarnation, the monoclonal antibody in the liquid pharmaceutical formulation is a human antibody. In one embodiment, the monoclonal antibody in the liquid pharmaceutical formulation is a human IgG1 antibody. In one of the incarnations, the monoclonal antibody in the liquid pharmaceutical formulation is GM37 variant 2. In another embodiment, the monoclonal antibody in the liquid pharmaceutical formulation includes a fixed heavy chain domain as defined in Serial ID number : 18 And a fixed range for the Kappa light chain as defined in Serial ID number : 17 . In one of the embodiments, the tensing agent in the liquid pharmaceutical formulation is chosen from mannitol, sorbitol, lactose, dextrose, trehalose, sodium chloride (NaCl), potassium chloride (KCl), glycerol, or glycerol. In one of the incarnations, the stress factor in the liquid pharmaceutical formulation is sodium chloride (NaCl). In one embodiment, the tensile agent in the liquid pharmaceutical formulation is sodium chloride (NaCl) at a concentration of approximately 70-140 millimolar. In one embodiment, the tensile agent in the liquid pharmaceutical formulation is sodium chloride (NaCl) at a concentration of approximately 50-150 millimolar. In one embodiment, the tensile agent in the liquid pharmaceutical formulation is sodium chloride (NaCl) at a concentration of approximately 100 millimolar. In one of the embodiments, the surfactant in the liquid pharmaceutical formulation is chosen from polysorbate 20 (Tween 20), polysorbate 80 (Tween 80), poloxamer 188, or Triton X-100. In one embodiment, the surfactant in the liquid pharmaceutical formulation Polysorbate 80 (Tween 80) is present in an amount between 0.02% and 0.05% (w / v). In one embodiment, the surfactant in the liquid pharmaceutical formulation is polysorbate 80 (Tween 80) in an amount of approximately 0.02% (w / v). In one embodiment, the tensile agent in the liquid pharmaceutical formulation is sodium chloride (NaCl), and the surfactant is polysorbate 80 (Tween 80). In one of the formulations, the concentration of histidine buffer in the liquid pharmaceutical formulation is between 25-40 millimoles. In one of the formulations, the concentration of histidine buffer in the liquid pharmaceutical formulation is approximately 25 millimoles. In one of the incarnations, the pH of the liquid pharmaceutical formulation is 6.0. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 30-225 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 30-200 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 30-150 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 30-100 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 45-55 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 50 mg / ml. In one formulation, the concentration of the anti-alpha-synuclein monoclonal antibody in the liquid pharmaceutical formulation is approximately 53 mg / ml. In one of the incarnations, the liquid pharmaceutical formulation in any of the above incarnations includes, in addition, at least one bulking agent chosen from sucrose, trehalose, glucose, lactose, sorbitol, mannitol, glycerol, arginine, aspartic acid, glutamic acid, glutamate, lysine, glycine, histidine, methionine, alanine, gelatin, PVP, PLGA, PEG, dextran, cyclodextrin and its derivatives, starch derivatives, HSA, or BSA. In one embodiment, the bulking agent in the liquid pharmaceutical formulation is arginine, glutamate, sucrose, glycine, or sorbitol at a concentration of 100-200 millimolar. In one embodiment, the bulking agent in the liquid pharmaceutical formulation is sucrose at a concentration of 100 millimolar. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), and 0.02% polysorbate 80 (Tween 80) (w / v) at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), 0.02% polysorbate 80 (Tween 80) (w / v), and water at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation includes 53 ±5 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), and 0.20 mg / ml of polysorbate 80 (Tween 80) at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 ±5 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), 0.20 mg / ml of polysorbate 80 (Tween 80), and water at a pH of 6.0. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), and 0.02% polysorbate 80 (Tween 80) (w / v), or contains amounts of each component within + / - 10% of the stated values, and has a pH of 6.0 or within + / - 10% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), 0.02% polysorbate 80 (Tween 80) (w / v), and water, or contains amounts of each component within + / - 10% of the stated values, and has a pH of 6.0 or within + / - 10% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), and 0.20 mg / ml of polysorbate 80 (Tween 80), or contains amounts of each component within + / - 10% of the stated values, and has a pH of 6.0 or within + / - 10% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), 0.20 mg / ml of polysorbate 80 (Tween 80), and water, or contains amounts of each component within + / - 10% of the stated values, and has a pH of 6.0 or within + / - 10% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), and 0.02% polysorbate 80 (Tween 80) (w / v), or contains amounts of each component within + / - 5% of the stated values, and has a pH of 6.0 or within + / - 5% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), 0.02% polysorbate 80 (Tween 80) (w / v), and water, or contains amounts of each component within + / - 5% of the stated values, and has a pH of 6.0 or within + / - 5% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), and 0.20 mg / ml of polysorbate 80 (Tween 80), or contains amounts of each component within + / - 5% of the stated values, and has a pH of 6.0 or within + / - 5% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), 0.20 mg / ml of polysorbate 80 (Tween 80), and water, or contains amounts of each component within + / - 5% of the stated values, and has a pH of 6.0 or within + / - 5% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), and 0.02% polysorbate 80 (Tween 80) (w / v), or contains amounts of each component within + / - 1% of the stated values, and has a pH of 6.0 or within + / - 1% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, 100 mM of sodium chloride (NaCl), 0.02% polysorbate 80 (Tween 80) (w / v), and water, or contains amounts of each component within + / - 1% of the stated values, and has a pH of 6.0 or within + / - 1% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), and 0.20 mg / ml of polysorbate 80 (Tween 80), or contains amounts of each component within + / - 1% of the stated values, and has a pH of 6.0 or within + / - 1% of the stated value. In one embodiment, the liquid pharmaceutical formulation consists mainly of 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 1.40 mg / ml of L-histidine, 3.34 mg / ml of L-histidine monohydrochloride, 34.16 mg / ml of sucrose, 5.83 mg / ml of sodium chloride (NaCl), 0.20 mg / ml of polysorbate 80 (Tween 80), and water, or contains amounts of each component within + / - 1% of the stated values, and has a pH of 6.0 or within + / - 1% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, and 100 mM of sodium chloride (NaCl), or contains amounts of each component within + / - 20% of the stated values, and 0.02% of polysorbate 80 (Tween 80) (w / v), or has a concentration within + / - 30% of the stated concentration, and has a pH of 6.0 or within + / - 20% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, and 100 mM of sodium chloride (NaCl), or contains amounts of each component within + / - 15% of the stated values, and 0.02% of polysorbate 80 (Tween 80) (w / v), or has a concentration within + / - 25% of the stated concentration, and has a pH of 6.0 or within + / - 15% of the stated value. In one embodiment, the liquid pharmaceutical formulation includes 53 mg / ml of anti-alpha-synuclein monoclonal antibody, 25 mM of histidine buffer, 100 mM of sucrose, and 100 mM of sodium chloride (NaCl), or contains amounts of each component within + / - 10% of the stated values, and 0.02% of polysorbate 80 (Tween 80) (w / v), or has a concentration within + / - 20% of the stated concentration, and has a pH of 6.0 or within + / - 10% of the stated value. In one of the incarnations, the liquid pharmaceutical formulation is a stable liquid pharmaceutical formulation. In one of the incarnations, the liquid pharmaceutical formulation is a low-viscosity liquid pharmaceutical formulation. It shall be understood that one or more features of any embodiments disclosed herein may be synthesized and / or rearranged within the scope of the invention to produce other embodiments that also fall within the scope of the invention. All embodiments are intended to apply to all aspects of this invention. Specific numbered incarnations: 1. A method for treating multiple system atrophy (MSA), where the aforementioned method involves administering an anti-alpha-synuclein monoclonal antibody intravenously to a person undergoing treatment with MSA, at a dose ranging between 4000 mg and 7000 mg or between 2000 mg and 4300 mg, where the aforementioned anti-alpha-synuclein monoclonal antibody binds to an epitope located within amino acids 112-117 (sequence identification number: 9 (ILEDMP)) of human alpha-synuclein (sequence identification number: 10). 2. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has early-onset MSA. 3. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has MSA in an early stage. 4. Treatment method for MSA according to any of the incarnations 1-3, where the total score on the UMSARS scale of a person undergoing treatment is less than 40. 5. Treatment of MSA according to any of the incarnations 1-4, where the total score on the UMSARS scale of a person undergoing treatment is less than 40 at the start of treatment. 6. Treatment of MSA according to any of the incarnations 1-4, where the total score on the UMSARS scale in a person undergoing treatment is less than 40 at the first administration of the antibody. 7. Treatment method for MSA according to incarnation 1, where the person undergoing treatment is suffering from MSA-C. 8. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has early MSA-C disease. 9. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has MSA-C in an early stage. 10. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has MSA-C and the total score on the UMSARS scale is less than 40. 11. Treatment method for MSA according to incarnation 1, where the person undergoing treatment has MSA-C and the total score on the UMSARS scale is less than 40 at the start of treatment. 12. Treatment of MSA according to incarnation 1, where the person being treated has MSA-C and the total score on the UMSARS scale is less than 40 at the first administration of the antibody. 13. Treatment of MSA according to any of the 1-12 incarnations, where the aforementioned monoclonal antibody includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . 14. Treatment of MSA according to any of the incarnations 1-13, where the said monoclonal antibody includes a variable heavy chain domain Serial ID number : 31 and a variable range for the light chain Serial ID number : 8 . 15. Treatment of MSA according to any of the incarnations 1-13, where the said monoclonal antibody includes a variable heavy chain domain Serial ID number : 31 and a variable range for the light chain Serial ID number : 8 . 16. Treatment method for MSA according to any of the incarnations 1-15, where the monoclonal antibody mentioned is a human antibody. 17. Treatment of MSA according to any of the incarnations 1-16, where the monoclonal antibody mentioned is a human IgG1 antibody. 18. Treatment method for MSA according to any of the incarnations 1-17, where the monoclonal antibody mentioned is GM37 variant 2 (Amlenetug). 19. Treatment of MSA according to any of the incarnations 1-18, where the said monoclonal antibody includes a stable heavy chain domain Serial ID number : 18 And a fixed range for the Kappa light chain Serial ID number : 17 . 20. Treatment of MSA according to any of the incarnations 1-19, whereby the aforementioned monoclonal antibody is given approximately every 4 weeks or approximately once a month. 21. Treatment of MSA according to any of the incarnations 1-20, whereby the aforementioned monoclonal antibody is given at a dose of approximately 2100 mg or approximately 4200 mg. 22. Treatment of MSA according to any of the incarnations 1-21, whereby the aforementioned monoclonal antibody is given at a dose of approximately 2100 mg. 23. Treatment of MSA according to any of the incarnations 1-21, whereby the aforementioned monoclonal antibody is given at a dose of approximately 4200 mg. 24. The treatment method for MSA according to any of the incarnations 1-23, where the treatment consists of delaying the progression of the disease. 25. Treatment method for MSA according to any of the incarnations 1-23, where the treatment consists of delaying clinical progression. 26. The treatment method for MSA according to any of the incarnations 1-23, where the treatment consists of slowing down the progression of the disease. 27. The treatment method for MSA according to any of the incarnations 1-23, where the treatment consists of slowing down clinical progression. 28. The treatment method for MSA according to any of the incarnations 1-27, whereby the treatment consists of delaying or slowing down the progression of the disease or clinical progression by not less than 5%, such as at least 10%, or at least 15%, or at least 20%, or at least 25%, or at least 30%, or at least 35%, or at least 40%, or at least 45%, or at least 50%, or at least 55%, or at least 60%, or at least 65%, or at least 70%, or at least 75%, or at least 80%, or at least 85%, or at least 90%. 29. The treatment of MSA according to any of the embodiments 1-28, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in any of the relevant Unified Multiple Systemic Atrophy Rating Scale (UMSARS) scores or any relevant parts of such scales, such as Part I, Part II, Part III or Part IV, or any single item of any of such scales or change from baseline in any combination of such UMSARS scales or any combination of single items of such UMSARS scales. 30. Treatment of MSA according to any of the incarnations 1-29, where the effect of treatment is quantified by longitudinal changes compared to baseline in the first and / or second part of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS), the first part of the Modified UMSARS Scale (mUMSARS), or the abbreviated UMSARS Scale (aUMSARS). 31. Treatment of MSA according to any of the incarnations 1-30, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in the overall score of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS TS). 32. The treatment method for MSA is according to any of the incarnations 1-30, where the effect of the treatment is measured quantitatively by longitudinal changes compared to the baseline in the modified UMSARS scale (mUMSARS). 33. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI). 34. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the bridge. 35. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum white matter. 36. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is measured quantitatively by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum gray matter. 37. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA by at least approximately 19%, according to the overall UMSARS score. 38. Treatment of MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow the clinical progression of MSA by at least approximately 22%, according to the score of Part 1 of the UMSARS scale. 39. Treatment of MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow the clinical progression of MSA by at least approximately 17%, according to the score of Part II of the UMSARS scale. 40. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA by at least approximately 27%, according to the modified UMSARS score. 41. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA-C by at least approximately 50%, according to the modified UMSARS score. 42. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA-C by at least approximately 50%, according to the overall UMSARS score. 43. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA-C by at least approximately 57%, according to the UMSARS Part 1 score. 44. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression of MSA-C by at least approximately 41%, according to the UMSARS Part II score. 45. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression in early MSA by at least approximately 42%, according to the modified UMSARS scale score. 46. ​​Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow down the clinical progression in early MSA by at least approximately 37%, according to the overall score of the UMSARS scale. 47. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the clinical progression in early MSA by at least approximately 42%, according to the score of Part I of the UMSARS scale. 48. Treatment of MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow down the clinical progression in early MSA by at least approximately 30%, according to the score of Part II of the UMSARS scale. 49. Treatment method for MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow down the local volumetric decrease in the bridge, with a volumetric decrease of no less than about 1.9%. 50. Treatment of MSA according to any of the incarnations 1-28, the effect of the treatment is to slow down the local volumetric decrease in the white matter of the cerebellum, with a volumetric decrease of at least about 3.3%. 51. Treatment of MSA according to any of the incarnations 1-28, the effect of the treatment is to slow down the local volumetric decrease in the gray matter of the cerebellum, with a volumetric decrease of at least about 1.5%. 52. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow down the local volumetric decrease in the bridge, with a volumetric decrease of at least about 2.4% less. 53. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow down the local volumetric decrease in the white matter of the cerebellum, with a volumetric decrease of at least about 4.2%. 54. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow down the local volumetric decrease in the gray matter of the cerebellum, with a volumetric decrease of at least about 0.4%. 55. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in MSA-C disease is to slow down the local volumetric decrease in the bridge, with a volumetric decrease of at least about 1.2%. 56. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in MSA-C disease is to slow the local volumetric decrease in the white matter of the cerebellum, with a volumetric decrease of at least about 3.8%. 57. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in MSA-C disease is to slow down the local volumetric decrease in the gray matter of the cerebellum, with a volumetric decrease of at least about 0.4%. 58. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow down the deterioration according to the measurement of the fourth part of the UMSARS scale - the overall disability score, with a decrease in the deterioration score of at least about 0.2. 59. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow the deterioration according to the measurement of the fourth part of the UMSARS scale - the overall disability score, with a decrease in the deterioration score of at least about 0.8. 60. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow down the deterioration according to the measurement of the overall clinical impression scale - disease severity, with a decrease in the degree of deterioration by at least about 0.2. 61. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow down the deterioration according to the measurement of the overall clinical impression scale - disease severity, with a decrease in the deterioration score of at least about 0.5. 62. Treatment of MSA according to any of the incarnations 1-28, where the effect of the treatment is to reduce the level of light chain of nerve fibers in the cerebrospinal fluid (CSF) by at least about 16.3%. 63. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA disease is to reduce the level of light chain of nerve fibers in the cerebrospinal fluid (CSF) by at least about 14.4%. 64. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment is to slow the deterioration according to the single item measurement “Speech” in the first part of the UMSARS scale, with a decrease in the degree of deterioration by at least about 0.4. 65. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow the deterioration according to the single item measure “Speech” in the first part of the UMSARS scale, with a decrease in the degree of deterioration of at least about 0.8. 66. Treatment of MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow the deterioration according to the single item measurement “Cutting food / Using cutlery” in the first part of the UMSARS scale, with a decrease in the deterioration score of at least about 0.3. 67. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow the deterioration according to the single item measurement “Cutting food / Using cutlery” in the first part of the UMSARS scale, with a decrease in the deterioration score of at least about 0.7. 68. Treatment method for MSA according to any of the incarnations 1-28, where the effect of the treatment is to slow down the deterioration according to the single item measurement “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the degree of deterioration of no less than about 0.3. 69. Treatment of MSA according to any of the incarnations 1-28, where the effect of treatment in early MSA is to slow the deterioration according to the single item measure “getting up from the chair” in Part II of the UMSARS scale, with a decrease in the deterioration score of at least about 1.2. 70. Treatment method for MSA according to any of the incarnations 1-69, where the monoclonal antibody is Amlenetug. Embodiment A1. Anti-alpha-synuclein monoclonal antibody for use in the treatment of multiple system atrophy (MSA), where the aforementioned use involves the intravenous administration of an anti-alpha-synuclein monoclonal antibody to a person under treatment with MSA, at a dose of between 4000 mg and 7000 mg or between 2000 mg and 4300 mg, where the aforementioned anti-alpha-synuclein monoclonal antibody is bound to an epitope located within amino acids 112-117 (Sequence ID: 9 (ILEDMP)) of human alpha-synuclein (Sequence ID: 10). Configuration A2. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has early MSA disease. Configuration A3. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has early-stage MSA. Embodiment A4. Anti-alpha-synuclein monoclonal antibody for use according to any of the embodiments A1-A3, where the total UMSARS score of a person undergoing treatment is less than 40. The A5 embodiment. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A4 embodiments, where the total UMSARS score of a person undergoing treatment is less than 40 at the start of treatment. Embodiment A6. Anti-alpha-synuclein monoclonal antibody for use according to any of the embodiments A1-A4, where the total UMSARS score of a person undergoing treatment is less than 40 at the first administration of the antibody. Configuration A7. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has MSA-C disease. Configuration A8. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has early MSA-C disease. Configuration A9. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has early-stage MSA-C. Configuration A10. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has MSA-C disease and the total UMSARS score is less than 40. Configuration A11. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has MSA-C disease and the total UMSARS score is less than 40 at the start of treatment. Configuration A12. Anti-alpha-synuclein monoclonal antibody for use according to Configuration A1, where the person being treated has MSA-C disease and the total UMSARS score is less than 40 at first administration of the antibody. Configuration A13. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A12 configurations, where the said monoclonal antibody includes: a. The CDR1 region of the heavy chain has an amino acid sequence. Serial ID number :1 ; b. The CDR2 region of the heavy chain has an amino acid sequence. Serial ID number : 34 ; c. The CDR3 region of the heavy chain has an amino acid sequence. Serial ID number : 3 ; d. The CDR1 region of the light chain has the following amino acid sequence. Serial ID number : 4 ; e. The CDR2 region of the light chain has the following amino acid sequence. Serial ID number : 5 ; and The CDR3 region of the light chain has the following amino acid sequence. Serial ID number :6 . Configuration A14. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A13 configurations, where the said monoclonal antibody includes a variable heavy chain domain. Serial ID number : 31 and a variable range for the light chain Serial ID number : 8 . Configuration A15. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A13 configurations, where the said monoclonal antibody includes a variable heavy chain domain. Serial ID number : 31 and a variable range for the light chain Serial ID number : 8 . Incarnation A16. Anti-alpha-synuclein monoclonal antibody for use in accordance with any of the incarnations A1-A15, where the monoclonal antibody said is a human antibody. Incarnation A17. Anti-alpha-synuclein monoclonal antibody for use in accordance with any of the incarnations A1-A16, where the monoclonal antibody said is a human IgG1 antibody. Incarnation A18. Anti-alpha-synocline monoclonal antibody for use according to any of the incarnations A1-A17, where the monoclonal antibody said is GM37 variant 2 (Amlenetug). Configuration A19. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A18 configurations, where the said monoclonal antibody includes a fixed heavy chain domain. Serial ID number : 18 And a fixed range for the Kappa light chain Serial ID number : 17 . Incarnation A20. Anti-alpha-synoclane monoclonal antibody for use according to any of the incarnations A1-A19, where the said monoclonal antibody is given approximately every 4 weeks or approximately once a month. The A21 incarnation. The anti-alpha-synoclane monoclonal antibody is for use according to any of the A1-A20 incarnations, where the said monoclonal antibody is given at a dose of approximately 2100 mg or approximately 4200 mg. The A22 incarnation. The anti-alpha-synoclane monoclonal antibody is for use according to any of the A1-A21 incarnations, where the said monoclonal antibody is given at a dose of approximately 2100 mg. The A23 incarnation. The anti-alpha-synoclane monoclonal antibody is for use according to any of the A1-A21 incarnations, where the said monoclonal antibody is given at a dose of approximately 4200 mg. Introduction A24. Anti-alpha-synoclane monoclonal antibody for use according to any of the A1-A23 introductions, where the treatment consists of delaying disease progression. Introduction A25. Anti-alpha-synoclane monoclonal antibody for use according to any of the A1-A23 introductions, where treatment consists of delaying clinical progression. Introduction A26. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A23 introductions, where the treatment consists of slowing disease progression. Introduction A27. Anti-alpha-synoclane monoclonal antibody for use according to any of the A1-A23 introductions, where the treatment consists of slowing clinical progression. The A28 embodiment. The anti-alpha-synuclein monoclonal antibody is for use in accordance with any of the A1-A27 embodiments, where the treatment consists of delaying or slowing disease progression or clinical progression by not less than 5%, such as at least 10%, or at least 15%, or at least 20%, or at least 25%, or at least 30%, or at least 35%, or at least 40%, or at least 45%, or at least 50%, or at least 55%, or at least 60%, or at least 65%, or at least 70%, or at least 75%, or at least 80%, or at least 85%, or at least 90%. Embodiment A29. Anti-alpha-synoclane monoclonal antibody for use according to any embodiment A1-A28, where the effect of treatment is quantified by longitudinal changes compared to baseline in any of the relevant Unified Systemic Atrophy Rating Scale (UMSARS) scores or any relevant parts of such scales, such as Part I, Part II, Part III, or Part IV, or any single item of any of such scales, or a change compared to baseline in any combination of such UMSARS scales or any combination of single items of such UMSARS scales. Embodiment A30. Anti-alpha-synuclein monoclonal antibody for use according to any embodiment A1-A29, where treatment effect is quantified by longitudinal changes compared to baseline in the first and / or second part of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS), the first part of the Modified UMSARS Scale (mUMSARS), or the abbreviated UMSARS Scale (aUMSARS). Configuration A31. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A30 configurations, where the effect of treatment is quantified by longitudinal changes compared to baseline in the overall score of the Unified Multiple Systemic Atrophy Assessment Scale (UMSARS TS). The A32 embodiment. The anti-alpha-synoclane monoclonal antibody is for use according to any of the A1-A30 embodiments, where the effect of treatment is quantified by longitudinal changes compared to baseline in the modified UMSARS scale (mUMSARS). The A33 embodiment. The anti-alpha-synuclein monoclonal antibody is for use according to any of the A1-A28 embodiments, where the effect of treatment is quantified by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI). Introduction A34. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A28 introductions, where the effect of treatment is quantified by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the bridge. Introduction A35. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A28 introductions, where the effect of treatment is quantified by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum white matter. Introduction A36. Anti-alpha-synuclein monoclonal antibody for use according to any of the A1-A28 introductions, where the effect of treatment is quantified by longitudinal changes compared to baseline in brain volume, using volumetric magnetic resonance imaging (vMRI) of the cerebellum gray matter. The A37 homologous anti-alpha-synuclein antibody is for use according to any of the A1-A28 homologs, where the therapeutic effect is to slow the clinical progression of MSA by at least approximately 19%, according to the overall UMSARS score. The A38 embodiment. The anti-alpha-synuclein monoclonal antibody is for use according to any of the A...

Claims

1. A method of treating early multiple system atrophy (MSA) or MSA-C, wherein said method comprises administering an effective amount of a monoclonal anti-alpha synuclein antibody to a human subject in need thereof, wherein said monoclonal anti-alpha synuclein antibody binds an epitope within amino acids 112-117 (SEQ ID NO:9 (ILEDMP)) of human alpha synuclein (SEQ ID NO:10), and wherein said monoclonal antibody comprises: a. a Heavy Chain CDR1 having the amino acid sequence of SEQ ID NO:1;b. a Heavy Chain CDR2 having the amino acid sequence of SEQ ID NO:34;c. a Heavy Chain CDR3 having the amino acid sequence of SEQ ID NO:3;d. a Light Chain CDR1 having the amino acid sequence of SEQ ID NO:4;e. a Light Chain CDR2 having the amino acid sequence of SEQ ID NO:5; andf. a Light Chain CDR3 having the amino acid sequence of SEQ ID NO:

6.   2. The method of treating MSA according claim 1, wherein the human subject has an UMSARS total score below 40 at treatment initiation.   3. The method of treating MSA according to any of claims 1-2, wherein the human subject has early MSA-C.   4. The method of treating MSA according to any one of claims 1-3, wherein the human subject has MSA-C and an UMSARS total score below 40 at treatment initiation.   5. The method of treating MSA according to any one of claims 1-4, wherein said monoclonal antibody comprises a heavy chain variable domain having the amino acid sequence of SEQ ID NO:31 and a light chain variable domain having the amino acid sequence of SEQ ID NO:8.  6. The method of treating MSA according to any one of claims 1-5, wherein said monoclonal antibody is a human IgG1 antibody.

7. The method of treating MSA according to any one of claims 1-6, wherein said monoclonal antibody comprises a constant heavy chain domain having the amino acid sequence of SEQ ID NO:18 and a kappa light chain constant domain having the amino acid sequence of SEQ ID NO:17.   8. The method of treating MSA according to any one of claims 1-7, wherein said monoclonal antibody is Amlenetug.    9. The method of treating MSA according to any one of claims 1-8, wherein said monoclonal antibody is administered intravenously about every 4 weeks.    10. The method of treating MSA according to any one of claims 1-8, wherein said monoclonal antibody is administered intravenously about once monthly.   11. The method of treating MSA according to any one of claims 1-10, wherein said monoclonal antibody is administered intravenously at a dose of about 2100 mg.    12. The method of treating MSA according to any one of claims 1-10, wherein said monoclonal antibody is administered intravenously at a dose of about 4200 mg.      13. The method of treating MSA according to any one of claims 1-12, wherein the treatment consists of slowing clinical progression by at least 5%, such as at least 10%, such as at least 15%, such as at least 20%, such as at least 25%, such as at least 30%, such as at least 35%, such as at least 40%, such as at least 45%, such as at least 50%, such as at least 55%, such as at least 60%, such as at least 65%, such as at least 70%, such as at least 75%, such as at least 80%, such as at least 85% or such as at least 90%.   14. The method of treating MSA according to any one of claims 1-13, wherein the treatment effect is quantified by longitudinal changes from baseline score using the Unified Multiple System Atrophy Rating Scale total score (UMSARS TS) or using the modified UMSARS (mUMSARS).   15. The method of treating MSA according to any one of claims 1-14, wherein the treatment effect is quantified by longitudinal changes from baseline in Brain Volume, as measured by Volumetric MRI (vMRI).

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