The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Mitochondria, Oxidative Damage, and Inflammation in Parkinson's Disease
Abstract
A bstract:The pathogenesis of Parkinson's disease (PD) remains obscure, but there is increasing evidence that impairment of mitochondrial function, oxidative damage, and inflammation are contributing factors. The present paper reviews the experimental and clinical evidence implicating these processes in PD. There is substantial evidence that there is a deficiency of complex I activity of the mitochondrial electron transport chain in PD. There is also evidence for increased numbers of activated microglia in both PD postmortem tissue as well as in animal models of PD. Impaired mitochondrial function and activated microglia may both contribute to oxidative damage in PD. A number of therapies targeting inflammation and mitochondrial dysfunction are efficacious in the MPTP model of PD. Of these, coenzyme Q 10 appears to be particularly promising based on the results of a recent phase 2 clinical trial in which it significantly slowed the progression of PD.
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Cites
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Cited by
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Mitochondrial Dysfunction and Oxidative Damage in parkin-deficient Mice
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Antioxidant assays for plant and food components
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Mitochondrial dysfunction and oxidative stress in Parkinson's disease
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Metadata
- Authors
- BEAL, M. F.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2003-06
- Volume
- 991
- Issue
- 1
- Pages
- 120-131
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2070895853
- Cited by
- 523
- References
- 14
- FWCI
- 24.23
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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