The amyloid hypothesis for Alzheimer's disease: a critical reappraisal.
The amyloid hypothesis has been the basis for most work on the pathogenesis of Alzheimer's disease. Recent clinical trials based on this hypothesis have been inconclusive. In this article I review the current status of the hypothesis and suggest that a major scientific need is to understand the normal function of amyloid-beta precursor protein (APP) and think how this may relate to the cell death in the disease process.
Hardy
John
J
Reta Lilla Weston Institute and Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK. j.hardy@ion.ucl.ac.uk
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D023582:Alzheimer Vaccines / Q000009:adverse effects; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002986:Clinical Trials as Topic / Q000379:methods / Q000592:standards; D018450:Disease Progression; D006801:Humans; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology
D023582:Alzheimer Vaccines; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor