Abstract
There is substantial evidence that mitochondrial dysfunction and oxidative damage may play a key role in the pathogenesis of neurodegenerative disease. Evidence supporting this in both Alzheimer's and Parkinson's diseases is continuing to accumulate. This review discusses the increasing evidence for a role of both mitochondrial dysfunction and oxidative damage in contributing to beta-amyloid deposition in Alzheimer's disease. I also discuss the increasing evidence that Parkinson's disease is associated with abnormalities in the electron transport gene as well as oxidative damage. Lastly, I reviewed the potential efficacy of coenzyme Q as well as a number of other antioxidants in the treatment of both Parkinson's and Alzheimer's diseases.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Alzheimer Disease / complications
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / metabolism*
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Animals
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Brain / drug effects
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Brain / metabolism
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Coenzymes
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Humans
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Mitochondria / drug effects
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Mitochondria / metabolism*
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Mitochondrial Diseases / complications
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Mitochondrial Diseases / drug therapy
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Mitochondrial Diseases / metabolism*
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Neurons / metabolism
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Neuroprotective Agents / therapeutic use
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Oxidation-Reduction
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Oxidative Stress / drug effects
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Parkinson Disease / drug therapy*
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Parkinson Disease / metabolism*
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Reactive Oxygen Species / metabolism
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Ubiquinone / analogs & derivatives*
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Ubiquinone / therapeutic use*
Substances
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Amyloid beta-Peptides
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Coenzymes
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Neuroprotective Agents
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Reactive Oxygen Species
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Ubiquinone
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coenzyme Q10