title: Society for Neuroscience--30th Annual Meeting. Alzheimer's disease: Therapeutics, targets and screens.
abstract: In the early 1990s, genetic mapping of the amyloid precursor protein (APP) locus and the markers linking it to FAD were recent discoveries. Since then, Alzheimer's disease (AD) research has progressed from the identification of FAD-linked mutation to the generation of transgenic animals that express these mutant genes. Transgenic animals can represent models of aberrant beta-amyloid (Abeta) production either through the expression of mutant APP genes or mutant presenilin (PS)-1 genes, or both. Currently, this plethora of well-characterized animal models is being applied to test candidate therapeutic agents and strategies to reverse or prevent amyloid deposition into plaques. Treatments included specific inhibitors of the enzymes that produce Abeta, non-steroidal anti-inflammatory therapies (NSAIDs), Abeta-chelating agents and dietary supplements.
authors: Baylor College of Medicine, Division of Neuroscience, Room S603, One Baylor Plaza, Houston, TX 77030, USA. kdineley@cns.bcm.tmc.edu
authors: K
authors: K
authors: Dineley