Induction of cellular oxidative stress by the beta-amyloid peptide involved in Alzheimer's disease.
Beta-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of beta-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating beta-amyloid, but the cellular effects of beta-amyloid induced reactive oxygen species production have not been fully elucidated.
Gibson
Gillian L
GL
Neurodegeneration Unit, Basic Medical Sciences, St. George's Hospital Medical School, Cranmer Terrace, Tooting, London SW17 0RE, UK.
Allsop
David
D
Austen
Brian M
BM
D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D045744:Cell Line, Tumor; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006801:Humans; D009447:Neuroblastoma / Q000201:enzymology / Q000378:metabolism / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments / Q000737:chemistry / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase