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From the Departments of Neurology (A.B., M.E., Y.S., F.G., T.K.), Nuclear Medicine (W.K., K.T.), and Pharmacology (M.M.), Klinikum Grosshadern, University of Munich, Germany; Max-Planck Institute for Psychiatry (B.M.-M.), Munich, Germany; and Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany (T.G.)
Address correspondence and reprint requests to Dr. Thomas Klopstock, Department of Neurology, Klinikum Grosshadern, University of Munich, Marchioninistr. 15, 81377 Munich, Germany; e-mail: thomas.klopstock{at}med.uni-muenchen.de
Mitochondrial dysfunction plays a major role in the pathogenesis of Parkinson disease (PD). Creatine (Cr) is an ergogenic compound that exerts neuroprotective effects in animal models of PD. We conducted a 2-year placebo-controlled randomized clinical trial on the effect of Cr in 60 patients with PD. Cr improved patient mood and led to a smaller dose increase of dopaminergic therapy but had no effect on overall Unified Parkinson's Disease Rating Scale scores or dopamine transporter SPECT.
T.G. and T.K. received a grant from the Wilhelm-Sander-Stiftung, Munich, Germany. Creatine monohydrate was kindly provided by SKW Trostberg, Germany.
Disclosure: The authors report no conflicts of interest.
Received December 21, 2005. Accepted in final form June 20, 2006.
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