Can a Daily Dose of Creatine Prevent Neurodegeneration

Creatine, increasingly popular as a dietary and exercise supplement,
has shown the ability to counteract laboratory models of amyotrophic lateral sclerosis
(ALS, or Lou Gehrig’s disease), Huntington’s disease, and Parkinson’s disease.
A significant new study shows that it slows the pathological and behavioral effects
of a transgenic model of Huntington’s disease, an autosomal dominant neurodegenerative
disorder that has both motor and mental effects.

In the June 15 issue of the Journal of Neuroscience, Robert Ferrante, Flint
Beal and associates describe experiments in which they added creatine supplement
to the feed of mice expressing part of the human Huntington’s gene. These mice
typically show physiological and behavioral signs resembling human Huntington’s
at an early age. In the mice fed creatine, there was significant protective
effect by a number of measures, e.g., increased length of survival, decreased
overall brain atrophy and body weight loss, delayed atrophy of striatal neurons,
delayed formation of aggregates of the gene product huntingtin, and improved
motor performance.

The idea behind using creatine in Huntington’s, as well as other neurodegenerative
diseases, is that these disorders may interfere with energy metabolism and thereby
initiate apoptotic mechanisms. Creatine, in the form creatine phosphate, functions
like ATP, storing high-energy phosphate bonds. It has been suggested that supplemental
creatine can thus help buffer against energy metabolism perturbations caused
by neurodegenerative disease processes, including those caused by Alzheimer’s.-Hakon Heimer.

Comment by Ethan Signer-Cure HD Initiative
This latest in a series of studies on creatine from the Beal group demonstrates
a benefit in a transgenic mouse model of Huntington’s disease (HD), similar
to that seen in their earlier work with a transgenic mouse model of amyotrophic
lateral sclerosis (ALS) and pharmacological mouse models of HD and Parkinson’s
disease (PD). The benefit is substantial if modest, including improvement in
a variety of behavioral and metabolic markers as well as a 20 percent increase in survival,
although the inverted dose-response curve remains puzzling. The extent of the
benefit and its effect on neurodegenerative diseases as different genetically
as HD, ALS and PD presumably reflect mitigation of compromised energy metabolism
that is secondary to the primary gene defect, and therefore suggest creatine
could benefit other neurodegenerative diseases (such as Alzheimer’s disease )
as well. Although a definitive trial of creatine in HD itself has yet to be
carried out, it is significant that creatine is considered completely safe for
humans and is widely available over the counter without prescription.

Ethan R. Signer
Professor of Biology Emeritus, MIT
Executive Director, Cure HD Initiative, Hereditary Disease Foundation
230 Park Avenue, 7th floor
New York, NY 10169
tel 917/368-5498 fax 917/368-5499
signer@mit.edu

Reference:Ferrante RJ, Andreassen OA, Jenkins BG, Dedeoglu A, Kuemmerle S, Kubilus JK, Kaddurah-Daouk R, Hersch SM, Beal MF. Neuroprotective effects of
creatine in a transgenic mouse model of Huntington’s disease. J Neurosci 2000 Jun 15;20(12). Abstract


To view commentaries, primary articles and linked stories, go to the original posting on Alzforum.org here.

Copyright © 1996–2017 Biomedical Research Forum, LLC. All Rights Reserved.

Share this:
Facebooktwittergoogle_plusmailFacebooktwittergoogle_plusmail