Life Extension Update
NIH to try creatine in Parkinson’s disease
The National Institutes of Health (NIH) National Institute of Neurological Disorders and Stroke (NINDS) is recruiting 1720 individuals for one of the largest Parkinson’s disease clinical trials to date, which will seek to determine if creatine slows the disease’s progression. Creatine is a nutritional supplement used by athletes and others to enhance exercise performance. The compound was identified by Parkinson’s disease researchers as having potential to treat the disease via a new rapid screening method.
The double-blind, placebo-controlled, phase III trial will enroll participants with early-stage Parkinson’s disease at medical centers across the United States and Canada. The trial is the first large study in a series called NET-PD (NIH Exploratory Trials in Parkinson's Disease), whose goal is to find effective treatments. Half of the study’s subjects will receive creatine while the remainder will receive a placebo for five years, during which participants will be periodically assessed for disease progression.
"This study is an important step toward developing a therapy that could change the course of this devastating disease," NIH director Elias A. Zerhouni, MD, commented. "The goal is to improve the quality of life for people with Parkinson's for a longer period of time than is possible with existing therapies."
Research suggests that creatine can improve the function of the energy-producing organelles of the cell known as mitochondria, and provide an antioxidant benefit. Research in an animal model of Parkinson’s disease using creatine has shown a protective effect against the loss of cells affected by the disease. "Creatine, or any compound that may slow the progression of Parkinson’s disease, could have very important long-term benefits for people who are living with this disease," stated NINDS associate director for clinical trials John R. Marler, MD.
“We think it may help cells that are damaged or overworked,” explained Dr Kapil D. Sethi, who is the director of the Movement Disorders Program at the Medical College of Georgia, one of the 51 sites conducting the study. “By giving more energy to the cell, you are giving them a safety margin. If a cell is dying, it takes another route and that would be surviving.”
Medical College of Georgia will be participating in a similar study of coenzyme Q10 to be conducted later this year. Coenzyme Q10 is another nutritional supplement that is involved in the production of energy. Like creatine, it is also available over-the-counter. Even though the supplements are widely available, Dr Sethi believes that Parkinson’s disease patients will still want to participate in the trial. “They are willing to take the risk of being on placebo for the cause of science and to learn more about the disease,” he said. “They want to beat this disease and if they can’t, they want to help somebody else beat it.”
During Parkinson’s, cells in the parts of the brain that control movement and regulate mood are gradually destroyed. The primary defect in Parkinson’s is a loss of dopaminergic neurons (such as dopamine-producing neurons) in a part of the brain called the substantia nigra. Dopamine is a neurotransmitter that modulates movement (Purves D et al 2001). In Parkinson’s disease, the dopamine-producing nerve cells are destroyed by high levels of oxidative damage (Atasoy HT et al 2004; Ross GW et al 2004). There is evidence that this oxidative damage is, in turn, caused by defects in the cells’ mitochondria, or power-generating centers.
The ideal treatment for Parkinson’s disease would be a neuroprotective agent— a treatment that protects the brain. While no neuroprotective prescription agent has been found, studies suggest that high-dose coenzyme Q10 (CoQ10), a natural agent, may have neuroprotective properties. CoQ10 is known to support mitochondria by enhancing energy levels in the brain, as well as by acting as a powerful antioxidant. In one phase 2 clinical trial, CoQ10 significantly slowed the progression of Parkinson’s disease (Beal MF 2003).
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