title: Oxidative phosphorylation defects and Alzheimer's disease.
abstract: Abnormalities in cellular bioenergetics have been identified in patients with Alzheimer's disease (AD) as well as in patients with other neurodegenerative diseases. The most commonly reported enzyme abnormalities are in the pyruvate dehydrogenase complex, the alpha-ketoglutarate dehydrogenase complex, and oxidative phosphorylation (OXPHOS). Although genetic evidence supporting primary OXPHOS defects as a cause for AD is weak, functionally important reductions in OXPHOS enzyme activities appear to occur in AD and may be related to beta-amyloid accumulation or other neurodegenerative processes. Since reduced neuronal ATP may enhance susceptibility to glutamate toxicity, OXPHOS defects could play an important role in the pathophysiology of AD.
authors.affiliation: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Shoffner
mesh_terms: D000544:Alzheimer Disease / Q000201:enzymology* / Q000235:genetics*; D016229:Amyloid beta-Peptides / Q000235:genetics; D004272:DNA, Mitochondrial; D003576:Electron Transport Complex IV / Q000235:genetics; D018698:Glutamic Acid / Q000235:genetics; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D010085:Oxidative Phosphorylation
chemical_list: D016229:Amyloid beta-Peptides; D004272:DNA, Mitochondrial; D018698:Glutamic Acid; D003576:Electron Transport Complex IV