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Mitochondria, Oxidative Damage, and Inflammation in Parkinson's Disease

Authors

  • M. FLINT BEAL

    Corresponding author
    1. Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, New York 10021, USA
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Address for correspondence: M. Flint Beal, M.D., Chairman, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, Room F610, New York, NY 10021. Voice: 212-746-6575; fax: 212-746-8532. fbeal@med.cornell.edu

Abstract

Abstract: 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 Q10 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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