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Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease

Departments of Obstetrics and Gynecology (T.L.H., S.D., C.L., M.S., P.S.), Neurobiology (T.L.H., C.L., R.T.M., C.J.B.), Pharmacology (J.D.E., R.H.R.), Ophthalmology-Visual Science (C.J.B.), Psychiatry (D.E.R.), and Neurosurgery (D.E.R.), Yale University School of Medicine, New Haven, Connecticut 06520; Instituto Cajal (L.M.G.-S.), Consejo Superior de Investigaciones Cientificas, Madrid, Spain 28002; The Vollume Institute (M.A.C.), Oregon Health & Science University, Portland, Oregon 97006; Department of Anatomy and Histology (T.L.H., P.S.), Szent Istvan University, Faculty of Veterinary Sciences, Budapest 1078, Hungary; and The St. Kitts Biomedical Research Foundation (E.H.D., D.E.R.), St. Kitts-Nevis, West Indies

Address all correspondence and requests for reprints to: Tamas L. Horvath, Department of Obstetrics/Gynecology, Yale Medical School, 333 Cedar Street, FMB 339, New Haven, Connecticut 06520. E-mail: tamas.horvath{at}yale.edu

Parkinson’s disease is characterized by dopamine cell loss of the substantia nigra. Parkinson’s disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.