30 results about "Cerebral amyloid angiopathy" patented technology

The present invention features non-human transgenic animal models for Alzheimer's disease (AD) and CAA, wherein the transgenic animal is characterized by 1) overexpression of bioactive transforming growth factor-beta1 (TGF-beta1) or 2) both overexpression of bioactive TGF-beta1 and expression of a human amyloid beta precursor protein (APP) gene product. The transgenic animals may be either homozygous or heterozygous for these alterations. Bigenic animals are further characterized by development of AD-associated and/or CAA-associated pathology within about two to three months of age.

Provided are methods for treating inflammatory neurodegenerative diseases (e.g., multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, stroke/cerebral ischemia, head trauma, spinal cord injury, Huntington's disease, migraine, cerebral amyloid angiopathy, inflammatory neurodegenerative condition associated with AIDS, age-related cognitive decline; mild cognitive impairment and prion diseases in a mammal), or at least one symptom thereof in a subject by administering a therapeutic composition comprising at least one electrokinetically-altered fluids (e.g., electrokinetically-generated oxygen-enriched fluids) of the present invention. Particular aspects provide methods for inhibiting and/or modulating the function and/or activity of effector T-cells, and/or for cell-based tolerogenic therapy (e.g., by modulating development and/or function and/or activity of T_REG cells and/or dendritic cells (DCs) and/or T_H17 cells (e.g., RORγt⁺ T_H17 cells). In certain aspects such methods comprise ex vivo exposure of T-cells and/or APC (e.g., dendridic cells) to at least one electrokinetically-altered fluid as disclosed herein. Combination therapies are additionally provided.

While the extracellular accumulation of amyloid-beta in the brain parenchyma is a pathological hallmark of Alzheimer's disease, its role as a cause or a consequence of AD is still debated. As described herein, intracellular Abeta1-42 is shown to be selectively toxic to neurons. The present invention provides methods of screening for compounds for the prevention and treatment of A amyloid associated diseases such as Alzheimer's disease, Down's Syndrome, cerebral amyloid angiopathy, and inclusion body myositis.

The invention provides a 2-aryl benzothiazole compound with high affinity with A(beta) plaque and a preparation method and application thereof. The structure of the compound is shown by formula (I). In-vitro competitive binding experiments indicate that the kind of molecules have medium affinity with the A(beta) 1-42 aggregate; in-vitro autoradiography experiments indicate that the molecules marked by Tc-99m can be combined with the A(beta) plaque in blood vessels of the brain with specificity and high affinity; in-vivo bio-distribution experiments on a normal mice indicate that a developer partially marked by Tc-99m has the advantages of low initial brain extraction, fast blood removal and the like, and is expected to become a new single-photon A(beta) plaque developer for early-stage clinical diagnosis of CAA (cerebral amyloid angiopathy) or AD (Alzheimer's disease).

The described invention relates to methods for treating, preventing, or diagnosing the pathology of progressive cognitive disorders resulting from accumulation of an amyloid peptide, in particular, Alzheimer's disease, Down's syndrome and cerebral amyloid angiopathy, in mammalian subjects using a composition comprising therapeutically effective amount of a leptin, leptin mimic, leptin derivative, leptin agonist, or AMP-dependent protein kinase activator, alone, or in combination with, one or more lipolytic/antilipogenic compounds. It further relates to methods for improving cognitive function using a composition comprising a therapeutically effective amount of leptin, a leptin mimic, a leptin derivative, an AMP-dependent protein kinase activator, a leptin agonist, a leptin blocker, a mimic of a leptin blocker, a leptin antagonist, an AMP-dependent protein kinase inhibitor; or a pharmaceutically acceptable salt thereof.

The disclosure relates to double stranded ribonucleic acid (dsRNAi) agents and compositions targeting the APP gene, as well as methods of inhibiting expression of an APP gene and methods of treating subjects having an APP-associated disease or disorder, such as cerebral amyloid angiopathy (CAA) and early onset familial Alzheimer disease (EOFAD or eFAD), using such dsRNAi agents and compositions.

The present disclosure encompasses compositions and methods for effectively treating at least one symptom or sign of A plaque or cerebral amyloid angiopathy (CAA) associated symptoms, or for decreasing amyloid plaque load or CAA load. The method comprises administering an effective amount of an anti-ApoE antibody to a mammalian subject, such as to a human.

The invention provides an in vitro method for diagnosing cerebral amyloid angiopathy (CAA), or for diagnosing or determining the risk of developing a complication of CAA, in a human subject, which method comprises analyzing serial dilutions of a plasma or serum sample of the subject, for determining at least one binding parameter of antibodies present therein, wherein said antibodies are anti-Aβ amyloid peptide(s) antibodies.

The present invention relates to a process for the preparation of a compound (I) or pharmaceutically acceptable salt thereof, which is useful as the key intermediate for the synthesis of compounds for prophylaxis and treatment of a disease associated with the deposition of β-amyloid in the brain, in particular Alzheimer's disease, and other diseases such as cerebral amyloid angiopathy, hereditary cerebral hemorrhage with amyloidosis, Dutch-type (HCHWA-D), multi-infarct dementia, dementia pugilistica and Down syndrome.

The invention provides application of Kenpaullone in preparation of a medicine capable of preventing or treating cerebral amyloid angiopathy. An experiment discovers that the Kenpaullone can increaseexpression of ADAM10 on a cell level but does not accelerate the expression of mRNA. In a further animal experiment APP/PS1 mouse model, a result discovers that the Kenpaullone obviously lightens cerebral vessel amyloid precipitation. An experiment proves for the first time that the Kenpaullone can increase the expression of the ADAM10, the amyloid metabolic pathway of APP can be converted into anon-amyloid metabolic pathway, and the generation of A[beta] which can be gathered and can precipitate is reduced. Research discovers that a Kenpaullone derivative Alsterpaullone(ALS) accelerates theprotein expression of the ADAM10 in SH-SY5Y cells; and AT7519 which is also CDK inhibitor does not affect the expression of the ADAM10 in SYSY5Y cells. All above research provides a clinical experiment guidance meaning for treatment of cerebral vessel amyloid degeneration and further medicine research and development.

This disclosure relates to an amyloid beta peptide (Aβ)-oligomer-specific antigen binding molecule and the use thereof as a diagnostic agent or as a therapeutic agent for the treatment or prevention of Alzheimer's Disease, Down's syndrome, mild cognitive impairment, cerebral amyloid angiopathy, vascular dementia, multi-infarct dementia, Parkinson's disease, Dementia with Lewy Bodies, Huntington's disease, Creutzfeldt-Jakob disease, cystic fibrosis, or Gaucher's disease.

The invention relates to novel 6-difluoromethyl-5,6-dihydro-2H-[1,4]oxazin-3-amine derivatives as inhibitors of beta-secretase, also known as beta-site amyloid cleaving enzyme, BACE, BACE1, Asp2, or memapsin2. The invention is also directed to pharmaceutical compositions comprising such compounds, to processes for preparing such compounds and compositions, and to the use of such compounds and compositions for the prevention and treatment of disorders in which beta-secretase is involved, such as Alzheimer's disease (AD), mild cognitive impairment, senility, dementia, dementia with Lewy bodies, cerebral amyloid angiopathy, multi-infarct dementia, Down's syndrome, dementia associated with stroke, dementia associated with Parkinson's disease and dementia associated with beta-amyloid.

Provided is a prevention or treatment agent for cerebral amyloid beta storage diseases, that contains a substance capable of suppressing the progression, alleviating the symptoms, and improving cerebral amyloid beta storage diseases. This prevention or treatment agent for cerebral amyloid beta storage diseases has as an effective component thereof a compound (e.g., Iguratimod) indicated by formula (1) or a salt thereof and, as a result, is capable of preventing or treating cerebral amyloid beta storage diseases such as Alzheimer-type dementia or cerebral amyloid angiopathy.

The invention discloses an application of a macrophage migration body as a cerebral amyloid vascular disease treatment target. According to the application disclosed by the invention, it is found for the first time that migratory bodies generated by A beta40-induced macrophages are related to pathophysiological processes of CAA, the migratory bodies derived from the macrophages damage blood-brain barriers in the CAA through complement-dependent cytotoxic effects, and macrophage apoptosis inhibition factors CD5L stop on blood vessel walls through the migratory bodies derived from the macrophages; the macrophage cell apoptosis inhibition factor CD5L can be used for promoting complement-dependent cytotoxic effect in CAA, so that the macrophage-derived migration body and the macrophage apoptosis inhibition factor CD5L can be used as new targets for CAA treatment. A reagent for inhibiting formation of macrophage migration bodies and expression of macrophage apoptosis inhibiting factors CD5L is developed to prepare a medicine for preventing and treating CAA, and compared with an immunosuppressor and glucocorticoid which are wide in action range, the reagent has the advantage of being high in targeting performance and small in side effects such as bleeding transformation, hepatorenal toxicity and A beta deposition.

The present disclosure relates to amyloid beta (Aβ) channels and the diseases and disorders caused by abnormal activity in these channels, such as Alzheimer's disease, Lewy body dementia, inclusion body myositis, or cerebral amyloid angiopathy. The disclosure provides compositions and methods that block Aβ channel activity and/or reduce Aβ-induced toxicity in a cell. Compositions comprised of compounds having histidine coordinating capacity are used in methods to prevent, reduce, or eliminate damage caused by Aβ ion channels.

The present invention relates to novel 5-(3-aminophenyl)-5-alkyl-5,6-dihydro-2H-[1,4]oxazin-3-amine derivatives as inhibitors of beta-secretase, also known as beta-site amyloid cleaving enzyme, BACE, BACE1, Asp2, or memapsin2. The invention is also directed to pharmaceutical compositions comprising such compounds, to processes for preparing such compounds and compositions, and to the use of such compounds and compositions for the prevention and treatment of disorders in which beta-secretase is involved, such as Alzheimer's disease (AD), mild cognitive impairment, senility, dementia, dementia with Lewy bodies, cerebral amyloid angiopathy, multi-infarct dementia, Down's syndrome, dementia associated with stroke, dementia associated with Parkinson's disease and dementia associated with beta-amyloid.