Human mitochondrial complex I dysfunction.

J M Cooper; V M Mann; D Krige; A H Schapira

doi:10.1016/s0005-2728(05)80019-2

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Human mitochondrial complex I dysfunction.

J M Cooper·V M Mann·D Krige·A H Schapira

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Abstract

In humans, complex I dysfunction has been observed in a high percentage of patients with mitochondrial myopathy. Analysis of mitochondria from these patients suggests the function and assembly of complex I is particularly susceptible to abnormalities of mitochondrial DNA, involving either point mutations of tRNA genes or major deletions. The evidence for a complex I defect in Parkinson's disease is accumulating, although the cause of this deficiency or the role it plays in the events that culminate in dopaminergic cell death remains unresolved.

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Aging Brain Diseases Chromosome Deletion DNA, Mitochondrial Humans Metabolic Diseases Mitochondria Muscular Diseases Mutation NAD(P)H Dehydrogenase (Quinone)Parkinson Disease Journal Article Research Support, Non-U.S. Gov't Review

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J M Cooper, V M Mann, D Krige, A H Schapira. 1992-07-17. Human mitochondrial complex I dysfunction.. https://doi.org/10.1016/s0005-2728(05)80019-2

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