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Mitochondrial amyloid-beta peptide: Pathogenesis or late-phase development?
Yan, Shirley ShiDu Xiong, Wen-Cheng Stern, David M.
Yan, Shirley ShiDu
Xiong, Wen-Cheng
Stern, David M.
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Abstract
Mitochondrial and metabolic dysfunction have been linked to Alzheimer's disease for some time. Key questions regarding this association concern the nature and mechanisms of mitochondrial dysfunction, and whether such changes in metabolic properties are pathogenic or secondary, with respect to neuronal degeneration. In terms of mitochondria and Alzheimer's, altered function could reflect intrinsic properties of this organelle, potentially due to mutations in mitochondrial DNA, or extrinsic changes secondary to signal transduction mechanisms activated in the cytosol. This review presents data relevant to these questions, and considers the implication of recent findings demonstrating the presence of amyloid-β peptide in mitochondria, as well as intra-mitochondrial molecular targets with which it can interact. Regardless of the underlying mechanism(s), it is likely that mitochondrial dysfunction contributes to oxidant stress which is commonly observed in brains of patients with Alzheimer's and transgenic models of Alzheimer's-like pathology.
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This is the publisher's version, also available electronically from http://iospress.metapress.com/content/8q4cf2u7gw6cllxt/?genre=article&issn=1387-2877&volume=9&issue=2&spage=127
Date
2006-07-17
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IOS Press
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Keywords
Respiratory chain complex, Alzheimer's disease, Neurodegeneration, Reactive oxygen species, Apoptosis
Citation
Yan, Shirley ShiDu et al. (2006). Mitochondrial amyloid-beta peptide: Pathogenesis or late-phase development? Journal of Alzheimer's Disease 9(2):127-37.