title: Preclinical detection of Parkinson's disease: biochemical approaches.
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.
authors.affiliation: Department of Neurology, University of Colorado School of Medicine, Denver.
authors.forename: W D
authors.initials: WD
authors.lastname: Parker
mesh_terms: D005609:Free Radicals; D006801:Humans; D016660:NAD(P)H Dehydrogenase (Quinone); D015418:Optic Atrophies, Hereditary; D010300:Parkinson Disease / Q000175:diagnosis* / Q000209:etiology; D010446:Peptide Fragments / Q000032:analysis; D011808:Quinone Reductases / Q000032:analysis / Q000502:physiology
chemical_list: D005609:Free Radicals; D010446:Peptide Fragments; D016660:NAD(P)H Dehydrogenase (Quinone); D011808:Quinone Reductases