Evidence for a defect in NADH: Ubiquinone oxidoreductase (Complex I) in Huntington’s disease

William Davis Parker; Sally J. Boyson; Anthony S. Luder; Janice K. Parks

doi:10.1212/wnl.40.8.1231

Evidence for a defect in NADH: Ubiquinone oxidoreductase (Complex I) in Huntington’s disease

William Davis Parker, Sally J. Boyson, Anthony S. Luder, Janice K. Parks

University of Colorado Anschutz Medical Campus

Research output: Contribution to journal › Article › peer-review

228 Scopus citations

Abstract

We evaluated electron transport chain activity in platelet mitochondria taken from HD patients. All 5 patients studied had striking depressions of NADH: ubiquinone oxidoreductase activity (complex I) (5.36 ± 2.91 nmol/min/mg; control mean, 19.12 ± 5.64 nmol/min/mg). Other electron transport chain activities were not significantly different from control values. HD may be caused by a mutation in 1 of the nuclear coded subunits of NADH: ubiquinone oxidoreductase.

Original language	English
Pages (from-to)	1231-1234
Number of pages	4
Journal	Neurology
Volume	40
Issue number	8
DOIs	https://doi.org/10.1212/wnl.40.8.1231
State	Published - Aug 1990
Externally published	Yes

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AB - We evaluated electron transport chain activity in platelet mitochondria taken from HD patients. All 5 patients studied had striking depressions of NADH: ubiquinone oxidoreductase activity (complex I) (5.36 ± 2.91 nmol/min/mg; control mean, 19.12 ± 5.64 nmol/min/mg). Other electron transport chain activities were not significantly different from control values. HD may be caused by a mutation in 1 of the nuclear coded subunits of NADH: ubiquinone oxidoreductase.

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Evidence for a defect in NADH: Ubiquinone oxidoreductase (Complex I) in Huntington’s disease

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