Abstract: The present invention relates to TP receptor antagonists, which have the ability to bind to TP receptor and optionally cross the blood brain barrier. The invention also provides compositions and methods for treating a disorder wherein activation of TP receptor is detrimental.

Abstract: The present invention is directed to methods of inhibiting a tauopathy in a patient by administration of a compound of formula I: Novel aminothienopyridazine compounds are also described.

Abstract: Provided are methods of assessing the absence or presence of a neurodegenerative disease in a subject comprising characterizing TDP-43 in a tissue sample of the subject. Also disclosed are methods for diagnosing a neurodegenerative disease in a subject, and methods for determining the efficacy of a drug against a neurodegenerative disease. Novel antibodies that bind to TDP-43 are also provided.

Abstract: The present invention is directed to compounds of formula I: wherein A is n is 0, 1, or 2; m is 0 or 1; R1 is H or C1-6alkyl and R2 is H, C1-6 alkyl, substituted or unsubstituted aryl, or substituted or unsubstituted heteroaryl; and X is O or N; as well as tautomers and pharmaceutically acceptable salt forms thereof. Uses of these compounds are also described.

Abstract: Provided is an antibody that selectively binds to an epitope formed by residues 1-11 of A? in an A? oligomer, a method comprising using the antibody to treat a disease characterized by such an A? amyloid deposit in a patient, and kits comprising same.

Abstract: Provided is a novel use of therapeutic concentrations of an inhibitor of glycogen synthase kinase-3 (GSK-3), including lithium or any other GSK-3 inhibitor, to block, reduce or inhibit processing of amyloid precursor proteins to beta-amyloid (A?) peptides, which are now believed to be the principal cause of Alzheimer's disease, thereby providing methods useful for the prevention, inhibition or reversal of the disease. Also provided are methods of using agents that specifically target the ? isoform of GSK-3, which is responsible for APP processing, making such selective GSK-3?-specific inhibitors especially useful in the treatment, prevention, and possible reversal of Alzheimer's disease. Further provided are kits and screening methods associated with the present methods.

Abstract: Provided are methods of assessing the absence or presence of a neurodegenerative disease in a subject comprising characterizing TDP-43 in a tissue sample of the subject. Also disclosed are methods for diagnosing a neurodegenerative disease in a subject, and methods for determining the efficacy of a drug against a neurodegenerative disease. Novel antibodies that bind to TDP-43 are also provided.

Abstract: Provided is a novel use of therapeutic concentrations of an inhibitor of glycogen synthase kinase-3 (GSK-3), including lithium or any other GSK-3 inhibitor, to block, reduce or inhibit processing of amyloid precursor proteins to beta-amyloid (A?) peptides, which are now believed to be the principal cause of Alzheimer's disease, thereby providing methods useful for the prevention, inhibition or reversal of the disease. Also provided are methods of using agents that specifically target the ? isoform of GSK-3, which is responsible for APP processing, making such selective GSK-3?-specific inhibitors especially useful in the treatment, prevention, and possible reversal of Alzheimer's disease. Further provided are kits and screening methods associated with the present methods.

Abstract: Methods of treating individuals suspected of suffering from diseases, conditions or disorders of the Central Nervous System including nerve damage are provided wherein stable, homogeneous post-mitotic human neurons are into the individual's brain or at or near a site of nerve damage. Pharmaceutical compositions of stable, homogeneous post-mitotic human neurons and a pharmaceutically acceptable medium are also disclosed. Methods of generating non-human animal models of human CNS diseases, conditions or disorders by implanting stable, homogeneous post-mitotic human neurons into the brain of a non-human animal are disclosed. Non-human animals eith stable, homogeneous post-mitotic human neurons implanted in their brain are also disclosed.

Abstract: Provided is a novel use of therapeutic concentrations of an inhibitor of glycogen synthase kinase-3 (GSK-3), including lithium or any other GSK-3 inhibitor, to block, reduce or inhibit processing of amyloid precursor proteins to beta-amyloid (A&bgr;) peptides, which are now believed to be the principal cause of Alzheimer's disease, thereby providing methods useful for the prevention, inhibition or reversal of the disease. Also provided are methods of using agents that specifically target the &agr; isoforn of GSK-3, which is responsible for APP processing, making such selective GSK-3&agr;-specific inhibitors especially useful in the treatment, prevention, and possible reversal of Alzheimer's disease. Further provided are kits and screening methods associated with the present methods.

Abstract: The present invention relates to transgenic animals expressing A53T &agr;-Syn protein which are models for neurodegenerative disease progression. These animals may be used for screening candidate drug compounds effective against neurodegenerative diseases and other diseases involving &agr;-synucleinopathy.

Abstract: &bgr; secretase pathways which process amyloid precursor protein into the amyloid peptides of neuritic plaques and vascular deposits that accumulate in the brains of patients with Alzheimer's disease have been identified in the endoplasmic reticulum of neuronal cells. Methods of identifying compounds which increase or decrease processing of amyloid precursor protein via these pathways which may be useful in the treatment of Alzheimer's disease and in identifying causative agents of this disease are provided.

Abstract: Methods of detecting RNA in brain tissue of patients with Alzheimer's disease are provided. Methods of diagnosing Alzheimer's disease by detection of these RNAs are also provided.

Abstract: Methods of detecting RNA in brain tissue of patients with Alzheimer's disease are provided. Methods of diagnosing Alzheimer's disease by detection of these RNAs are also provided.

Abstract: Methods of treating individuals suspected of suffering from diseases, conditions or disorders of the Central Nervous System which comprise implanting stable, homogeneous post-mitotic human neurons into the individual's brain are disclosed. Methods of treating individuals suspected of suffering from injuries, diseases, conditions or disorders characterized by nerve damage which comprise implanting stable, homogeneous post-mitotic human neurons at or near a site of said nerve damage. Pharmaceutical compositions comprising stable, homogeneous post-mitotic human neurons and a pharmaceutically acceptable medium are disclosed. Methods of generating non-human animal models of human CNS diseases, conditions or disorders which comprise implanting stable, homogeneous post-mitotic human neurons into the brain of a non-human animal are disclosed. Non-human animals comprising stable, homogeneous post-mitotic human neurons implanted in their brain are disclosed.

Abstract: Methods of detecting RNA in brain tissue of patients with Alzheimer's disease are provided. Methods of diagnosing Alzheimer's disease by detection of these RNAs are also provided.

Abstract: Methods of treating individuals suspected of suffering from diseases, conditions or disorders of the Central Nervous System which comprise implanting stable, homogeneous post-mitotic human neurons into the individual's brain are disclosed. Methods of treating individuals suspected of suffering from injuries, diseases, conditions or disorders characterized by nerve damage which comprise implanting stable, homogeneous post-mitotic human neurons at or near a site of said nerve damage are also disclosed.

Abstract: Methods of generating a rat having A.beta. deposits in the brain of the rat by injecting an amount of human A68 protein sufficient to result in formation of the deposits and subsequently examining the rat for the formation of the deposits are disclosed. Rats characterized by the presence of A.beta. deposits similar to those found in individuals with Alzheimer's disease are also disclosed. Methods of screening test compositions for prophylactic or therapeutic activity by generating a rat having A.beta. deposits in its brain, treating the animal with the test composition and examining the animal for therapeutic or prophylactic effectiveness are also disclosed.

Abstract: This invention relates to a method of imaging amyloid deposits and to labeled compounds, and methods of making labeled compounds useful in imaging amyloid deposits. This invention also relates to compounds, and methods of making compounds for inhibiting the aggregation of amyloid proteins to form amyloid deposits, and a method of delivering a therapeutic agent to amyloid deposits.

Abstract: This invention relates to a method of imaging amyloid deposits and to labeled compounds, and methods of making labeled compounds useful in imaging amyloid deposits. This invention also relates to compounds, and methods of making compounds for inhibiting the aggregation of amyloid proteins to form-amyloid deposits, and a method of delivering a therapeutic agent to amyloid deposits.