Affiliations: Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA | Neurology Service, VA Health Care System, San Diego, CA 92161, USA | Massachusetts General Hospital, Boston, MA, USA | Cornell‐New York Hospital, New York, NY 02114, USA
Note: [] Correspondence to: Cliff Shults, M.D., Neurology Service (9127), VA Medical Center, 3350 La Jolla Village Drive, San Diego, CA 92161, USA.
Abstract: Parkinson’s disease (PD) is a degenerative neurological disorder. Recent studies have demonstrated reduced activity of complex I of the electron transport chain in brain and platelets from patients with PD. Platelet mitochondria from parkinsonian patients were found to have lower levels of coenzyme Q_{10} (CoQ_{10}) than mitochondria from age/sex‐matched controls. There was a strong correlation between the levels of CoQ_{10} and the activities of complexes I and II/III. Oral CoQ_{10} was found to protect the nigrostriatal dopaminergic system in one‐year‐old mice treated with MPTP, a toxin injurious to the nigrostriatal dopaminergic system. We further found that oral CoQ_{10} was well absorbed in parkinsonian patients and caused a trend toward increased complex I activity. These data suggest that CoQ_{10} may play a role in cellular dysfunction found in PD and may be a potential protective agent for parkinsonian patients.
Journal: Biofactors, vol. 9, no. 2-4, pp. 267-272, 1999
