Amyloid beta-peptide [1-42]-associated free radical-induced oxidative stress and neurodegeneration in Alzheimer's disease brain: mechanisms and consequences.
In addition to synapse loss, neurofibrillary tangles, and neurodegeneration, oxidative stress and amyloid beta-peptide [Abeta] deposition are hallmarks of Alzheimer's disease [AD] brain. Our laboratory coupled these two characteristics of AD into a comprehensive model to account for the synapse loss and neurodegeneration in AD brain. This model combines much of the extant studies on AD and is based on oxidative stress associated with amyloid beta-peptide. This review presents evidence in support of this model and provides insight into the molecular basis of this devastating dementing disorder.
Butterfield
D Allan
DA
Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA. dabcns@uky.edu
D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000502:physiology*; D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D009410:Nerve Degeneration / Q000378:metabolism*; D018384:Oxidative Stress; D010446:Peptide Fragments / Q000502:physiology*
D016229:Amyloid beta-Peptides; D005609:Free Radicals; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)