title: Amyloid-beta-induced mitochondrial dysfunction.
abstract: As an important molecule in the pathogenesis of Alzheimer's disease (AD), amyloid-beta (Abeta) interferes with multiple aspects of mitochondrial function, including energy metabolism failure, production of reactive oxygen species (ROS) and permeability transition pore formation. Recent studies have demonstrated that Abeta progressively accumulates within mitochondrial matrix, providing a direct link to mitochondrial toxicity. Abeta-binding alcohol dehydrogenase (ABAD) is localized to the mitochondrial matrix and binds to mitochondrial Abeta. Interaction of ABAD with Abeta exaggerates Abeta-mediated mitochondrial and neuronal perturbation, leading to impaired synaptic function, and dysfunctional spatial learning/memory. Thus, blockade of ABAD/Abeta interaction may be a potential therapeutic strategy for AD.
authors.affiliation: Harvey Cushing Institutes of Neuroscience, North Shore-Long Island Jewish Health System, Great Neck, NY 11021, USA.
authors.forename: John Xi
authors.initials: JX
authors.lastname: Chen
authors.forename: Shi Du
authors.initials: SD
authors.lastname: Yan
mesh_terms: D000544:Alzheimer Disease / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D004734:Energy Metabolism; D006801:Humans; D028361:Mitochondrial Diseases / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology
chemical_list: D016564:Amyloid beta-Protein Precursor