Abstract: The construction of transgenic animal models of human Alzheimer's disease, and methods of using the models to screen potential Alzhe## disease therapeutics, are described. The models are characterized by pathologies similar to pathologies observed in Alzheimer's disease, based on expression of all three forms of the ?-amyloid precursor protein (APP), APP695, APP751, and APP770, as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer's disease (FAD) mutations at amino acid 717, predicted mutations in the APP gene, and truncated forms of APP that contain the A? region. Animal cells can be isolated from the transgenic animals or prepared using the same constructs with standard techniques such as lipofection or electroporation.

Abstract: The construction of transgenic animal models of human Alzheimer'disease, and methods of using the models to screen potential Alzheimer's disease therapeutics, are described. The models are characterized by pathologies similar to pathologies observed in Alzheimer's disease, based on expression of all three forms of the &bgr;-amyloid precursor protein (APP), APP695, APP751, and APP770, as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer's disease (FAD) mutations at amino acid 717, predicted mutations in the APP gene, and truncated forms of APP that contain the A&bgr; region. Animal cells can be isolated from the transgenic animals or prepared using the same constructs with standard techniques such as lipofection or electroporation.

Abstract: The construction of transgenic animal models of human Alzheimer's disease, and methods of using the models to screen potential Alzheimer's disease therapeutics, are described. The models are characterized by pathologies similar to pathologies observed in Alzheimer's disease, based on expression of all three forms of the &bgr;-amyloid precursor protein (APP), APP695, APP751, and APP770, as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer's disease (FAD) mutations at amino acid 717, predicted mutations in the APP gene, and truncated forms of APP that contain the A&bgr; region. Animal cells can be isolated from the transgenic animals or prepared using the same constructs with standard techniques such as lipofection or electroporation.

Abstract: Substituted pyrimidines that have the general structure: in which the symbol R1 represents a C1-C6 alkyl, C1-C6 alkoxy or halogen atom; R2 represents a phenyl group, substituted phenyl group, benzyl moiety, substituted benzyl moiety, C3-C7 cycloalkyl, or substituted C3-C7 cycloalkyl; R3 represents a hydrogen or C1-C6 alkyl group, R4 represents —H, —OH, —N3 or —NHCOCH3; and R5 represents H are provided. These compounds have activity as inhibitors of phospholipase A2, and are useful in treating disorders mediated by phospholipase A2.

Abstract: The construction of transgenic animal models of human Alzheimer's disease, and methods of using the models to screen potential Alzheimer's disease therapeutics, are described. The models are characterized by pathologies similar to pathologies observed in Alzheimer's disease, based on expression of all three forms of the &bgr;-amyloid precursor protein (APP), APP695, APP751, and APP770, as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer's disease (FAD) mutations at amino acid 717, predicted mutations in the APP gene, and truncated forms of APP that contain the A&bgr; region. Animal cells can be isolated from the transgenic animals or prepared using the same constructs with standard techniques such as lipofection or electroporation.

Abstract: Arylsulfonamides which have the general structure: with the symbols R.sup.1, R.sup.2, R.sup.3, R.sup.4, A and n representing the groups and integers provided in the detailed description are provided herein. These compounds have activity as inhibitors of phospholipase A2, inhibitors of cytokine release and as inhibitors of neurodegeneration.

Abstract: The invention is drawn to a method for identifying agents that inhibit neural degeneration by administering to cell populations consisting essentially of neurons or cells from neuronal cell lines, where these cells are exposed to an apoptotic stimulus other than APP gene products, an agent, where it is determined whether the agent inhibits neural degeneration.

Abstract: The invention provides methods and compositions for treating neurodegeneration in mammalian cells by administering a phospholipase A2 inhibitor.