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Neuroscience. 2007 Apr 14;145(4):1233-48. Epub 2007 Feb 14.

Oxidative stress and mitochondrial dysfunction in neurodegenerative diseases.

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1
Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.

Abstract

In recent years, it has become increasingly clear that mitochondrial dysfunction and oxidative damage are major contributors to neuronal loss. Free radicals, typically generated from mitochondrial respiration, cause oxidative damage of nucleic acids, lipids, carbohydrates and proteins. Despite enormous amount of effort, however, the mechanism by which oxidative damage causes neuronal death is not well understood. Emerging data from a number of neurodegenerative diseases suggest that there may be common features of toxicity that are related to oxidative damage. In this review, while focusing on Huntington's disease (HD), we discuss similarities among HD, Friedreich ataxia and xeroderma pigmentosum, which provide insight into shared mechanisms of neuronal death.

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