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- Publisher
- IOS Press
- Copyright
- IOS Press and the authors. All rights reserved
- ISSN
- 1387-2877
- eISSN
- 1875-8908
- DOI
- 10.3233/jad-2007-12208
- Publisher site
- See Article on Publisher Site
Abstract
As an important molecule in the pathogenesis of Alzheimer's disease (AD), amyloid-β (Aβ) 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 Aβ progressively accumulates within mitochondrial matrix, providing a direct link to mitochondrial toxicity. Aβ-binding alcohol dehydrogenase (ABAD) is localized to the mitochondrial matrix and binds to mitochondrial Aβ. Interaction of ABAD with Aβ exaggerates Aβ-mediated mitochondrial and neuronal perturbation, leading to impaired synaptic function, and dysfunctional spatial learning/memory. Thus, blockade of ABAD/Aβ interaction may be a potential therapeutic strategy for AD.
Journal
Journal of Alzheimer's Disease – IOS Press
Published: Jan 1, 1
Keywords: Alzheimer's disease; amyloid-β; mitochondria; energy metabolism; ABAD