Journal
NEUROCHEMICAL RESEARCH
Volume 33, Issue 12, Pages 2502-2509Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-008-9855-x
Keywords
Mitochondria; Mitochondrial DNA; Genes Parkinson's disease; Friedreich's ataxia; Oxidative stress
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Funding
- Medical Research Council [G0601943] Funding Source: researchfish
- Medical Research Council [G0601943] Funding Source: Medline
- MRC [G0601943] Funding Source: UKRI
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Mitochondria play a pivotal role in mammalian cell metabolism, hosting a number of important biochemical pathways including oxidative phosphorylation. As might be expected from this fundamental contribution to cell function, abnormalities of mitochondrial metabolism are a common cause of human disease. Primary mutations of mitochondrial DNA result in a diverse group of disorders often collectively referred to as the mitochondrial encephalomyopathies. Perhaps more importantly in numerical terms are those neurodegenerative diseases caused by mutations of nuclear genes encoding mitochondrial proteins. Finally there are mitochondrial abnormalities induced by secondary events e. g. oxidative stress that may contribute to senescence, and environmental toxins that may cause disease either alone or in combination with a genetic predisposition.
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