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From the Departments of Neurology (Drs. Parker and Boyson, and J.K. Parks) and Pediatrics (Drs. Parker and Luder), University of Colorado School of Medicine, Denver, CO.
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.
Address correspondence and reprint requests to Dr. W.D. Parker, Box C-233, Section of Pediatric Neurology, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262.
Supported by NIH grant NS25382 from NINDS (W.D.P.), a Mental Retardation Research Center Grant from NICHD, and a grant (RR-69) from the General Clinical Research Centers Program of the Division of Research Resources, National Institutes of Health. Dr. Parker and Dr. Boyson hold Clinical Investigator Development Awards from NINDS.
Received October 25, 1989. Accepted for publication in final form February 8, 1990.
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