Neurology®
The most widely read and highly cited peer-reviewed Neurology journal
Quick Search
Advanced Search
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Data Supplement
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hersch, S. M.
Right arrow Articles by Rosas, H. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hersch, S. M.
Right arrow Articles by Rosas, H. D.
Related Collections
Right arrow HIV
Right arrow All Clinical trials
Right arrow Clinical trials Randomized controlled (CONSORT agreement)
NEUROLOGY 2006;66:250-252
© 2006 American Academy of Neurology


Brief Communications

Creatine in Huntington disease is safe, tolerable, bioavailable in brain and reduces serum 8OH2'dG

S. M. Hersch, MD, PhD, S. Gevorkian, MSc, K. Marder, MD, MPH, C. Moskowitz, MS, A. Feigin, MD, M. Cox, MS, RN, P. Como, PhD, C. Zimmerman, RN, M. Lin, MD, L. Zhang, MD, A. M. Ulug, PhD, M. F. Beal, MD, W. Matson, PhD, M. Bogdanov, E. Ebbel, A. Zaleta, BA, Y. Kaneko, BA, B. Jenkins, PhD, N. Hevelone, MPH, H. Zhang, MS, H. Yu, MPH, D. Schoenfeld, PhD, R. Ferrante, PhD, MSc and H. D. Rosas, MD, MS

From the Departments of Neurology, (S.M.H., S.G., A.Z., N.H., H.Z., H.Y., H.D.R.) and Biostatistics (D.S.), MassGeneral Institute for Neurodegenerative Disease, MGH-NMR Center and Athinoula A. Martinos Center for Biomedical Imaging (A.Z., B.J., N.H., H.D.R.), Massachusetts General Hospital and Harvard Medical School, Charlestown, MA; Center for Parkinson's Disease and Other Movement Disorders (K.M., C.M.), Department of Neurology, Sergievsky Center and Taub Institute for Research on Alzheimer's Disease and the Aging Brain (K.M.), Columbia University, New York, NY; Center for Neuroscience, Institute for Medical Research (A.F., M.C.), North Shore-LIJ Health System, Manhasset, NY; Department of Neurology (P.C., C.Z.), University of Rochester, Rochester, NY; Departments of Neurology and Neuroscience (M.L., M.F.B., M.B.), and Radiology (L.Z., A.M.U.), Weill Medical College of Cornell University, New York, NY; Edith Nourse Veterans Administration Medical Center (W.M., M.B., E.E., R.F.), Geriatric Research and Education and Clinical Center, Bedford, MA; Departments of Neurology, Pathology, and Psychiatry (R.F.) and Biochemistry (W.M., R.F.), Boston University School of Medicine, Boston, MA.

Address correspondence and reprint requests to Dr. Steven Hersch, MassGeneral Institute for Neurodegenerative Disease, MGH East Building 114-2001, 114 16th Street, Charlestown, MA 02129; e-mail: hersch{at}helix.mgh.harvard.edu.

In a randomized, double-blind, placebo-controlled study in 64 subjects with Huntington disease (HD), 8 g/day of creatine administered for 16 weeks was well tolerated and safe. Serum and brain creatine concentrations increased in the creatine-treated group and returned to baseline after washout. Serum 8-hydroxy-2'-deoxyguanosine (8OH2'dG) levels, an indicator of oxidative injury to DNA, were markedly elevated in HD and reduced by creatine treatment.


Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the January 24 issue to find the title link for this article.

Supported by NIH/National Center for Complementary and Alternative Medicine grant AT00613, NIH/NINDS grants NS35255 and NS042861, and the Claflin Scholar's Fund. The MGH Mallinckrodt and Columbia University General Clinical Research Centers (M01-RR01066 and MO1-RR00645) provided support for clinical activities. Creatine monohydrate and placebo were provided by The Avicena Group, Inc. (Palo Alto, CA).

Disclosure: The authors report no conflicts of interest.

Received May 10, 2005. Accepted in final form October 12, 2005.




This article has been cited by other articles:


Home page
Hum Mol GenetHome page
R. K. Chaturvedi, P. Adhihetty, S. Shukla, T. Hennessy, N. Calingasan, L. Yang, A. Starkov, M. Kiaei, M. Cannella, J. Sassone, et al.
Impaired PGC-1{alpha} function in muscle in Huntington's disease
Hum. Mol. Genet., August 15, 2009; 18(16): 3048 - 3065.
[Abstract] [Full Text] [PDF]


Home page
JEMHome page
M. Bjorkqvist, E. J. Wild, J. Thiele, A. Silvestroni, R. Andre, N. Lahiri, E. Raibon, R. V. Lee, C. L. Benn, D. Soulet, et al.
A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease
J. Exp. Med., August 4, 2008; 205(8): 1869 - 1877.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
E. C. Stack, S. J. Del Signore, R. Luthi-Carter, B. Y. Soh, D. R. Goldstein, S. Matson, S. Goodrich, A. L. Markey, K. Cormier, S. W. Hagerty, et al.
Modulation of nucleosome dynamics in Huntington's disease
Hum. Mol. Genet., May 15, 2007; 16(10): 1164 - 1175.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
M. S Parihar and G. J. Brewer
Mitoenergetic failure in Alzheimer disease
Am J Physiol Cell Physiol, January 1, 2007; 292(1): C8 - C23.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
L. E. Meyer, L. B. Machado, A. P. S. A. Santiago, W. S. da-Silva, F. G. De Felice, O. Holub, M. F. Oliveira, and A. Galina
Mitochondrial Creatine Kinase Activity Prevents Reactive Oxygen Species Generation: ANTIOXIDANT ROLE OF MITOCHONDRIAL KINASE-DEPENDENT ADP RE-CYCLING ACTIVITY
J. Biol. Chem., December 8, 2006; 281(49): 37361 - 37371.
[Abstract] [Full Text] [PDF]