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Evidence for a defect in NADH: ubiquinone oxidoreductase (complex I) in Huntington's disease
W D Parker1, S J Boyson, A S Luder
1Department of Neurology, University of Colorado School of Medicine, Denver.
Neurology
|August 1, 1990
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.