Aging, amyloid, and Alzheimer's disease: a perspective in honor of Carl Cotman.
Deciphering the molecular basis of synaptic dysfuction in Alzheimer's disease (AD) has engaged the attention of scientists with diverse backgrounds and interests. The synthesis of experimental findings from neuropathology, biochemistry, genetics, animal modeling and even immunology, has provided a plausible model for the pathogenesis of the disorder. While not universally accepted, the so-called amyloid (or Abeta) hypothesis of AD is well supported scientifically and predicts several specific targets for therapeutic intervention. Some of these are now reaching the clinic, providing the final and most important test for this hypothetical mechanism of disease.
Selkoe
Dennis J
DJ
Center for Neurological Diseases, Brigham and Women's Hospital, and the Harvard Center for Neurodegeneration and Repair Boston, Massachusetts, USA. nboucher@rics.bwh.harvard.edu
D000375:Aging; D000544:Alzheimer Disease / Q000188:drug therapy / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000737:chemistry* / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D001923:Brain Chemistry; D006801:Humans; D009410:Nerve Degeneration / Q000378:metabolism* / Q000503:physiopathology; D009473:Neuronal Plasticity; D009435:Synaptic Transmission
D016229:Amyloid beta-Peptides