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Preclinical detection of Parkinson's disease

Biochemical approaches

From the Departments of Neurology and Pediatrics, University of Colorado School of Medicine, Denver.

Address correspondence and reprint requests to Dr. W. Davis Parker, Box C233, University of Colorado Health Sciences Center, Denver, CO 80262.

Abstract.

Dysfunction of NADH: ubiquinone oxidoreductase (complex I) of the mitochondrial electron transport chain has been linked to the pathogenesis of Parkinson's disease. While simple assays of complex I activity are unlikely to be useful in the preclinical detection of Parkinson's disease, other more sophisticated physical-chemical approaches including detection of free radical damage may have utility. Leber's hereditary optic neuropathy may provide a useful model system for development of such strategies.

Footnotes

This work was supported by NIH grant NS325382 from NINDS, 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.