Scientists Identify Mechanism for Caffeine’s Potential Protective Effect Against Parkinson’s Disease
For immediate release.
NEWS RELEASE NR-01-03 (sent 5/4).For more information, please call Joe Carey at 202-745-5138 or the MGH public affairs office, 617-724-6423.
SCIENTISTS IDENTIFY MECHANISM FOR CAFFEINE’S POTENTIAL PROTECTIVE EFFECT AGAINST PARKINSON’S DISEASE
WASHINGTON, D.C. May 4 — That morning cup of coffee may be doing a lot more than giving you a needed lift at the start of the day. In mice studies, scientists have found that caffeine is able to prevent the loss of the chemical signal that is depleted in Parkinson’s disease.
The study links caffeine's effects to the A2A receptor located on nerve cells next to those that degenerate in Parkinson's patients. A2A receptors, which bind the molecule adenosine, are found in distinct areas of the brain, and their expression is restricted to the very cells that are targets of the neurons that go awry in Parkinson's disease, which afflicts some 500,000 Americans.
Caffeine acts as an antagonist to the A2A receptor, blocking its binding site and rendering it inactive, notes lead author Michael Schwarzschild, MD, PhD, a neurologist at Boston’s Massachusetts General Hospital (MGH). The effects of caffeine were mimicked by several known A2A blockers as well as by genetic inactivation of the A2A receptor. The study, funded in part by the National Institutes of Health, appears in the May 15 issue of The Journal of Neuroscience.
“This report provides a scientific basis for understanding the reported inverse relationship between caffeine consumption and Parkinson's disease and points to the possible role of A2a adenosine blockers as potential disease modifying interventions,” says Ira Shoulson, MD, a neurologist at the University of Rochester.
The new mouse study adds to recent population studies showing that caffeine may be linked to a decreased risk of Parkinson’s. “The animal results lend more weight to caffeine’s neuroprotective nature,” says Schwarzschild. “But it doesn’t prove it. They do not provide a rationale for changing caffeine consumption habits.” Time will tell if the mouse data will translate to humans.
Dopamine replacement is the standard treatment for Parkinson's disease today. Despite this treatment, the disease continues to progress, often accompanied by motor side effects of the therapy. A2A receptor antagonists can enhance motor function and perhaps even slow disease progression without these complications. A2A receptor antagonists are now entering human trials for the treatment of Parkinson's disease.
Schwarzschild’s co-authors include Jiang-Fan Chen, MD, PhD, a co-director of the study project. Both are members of the Society for Neuroscience, an organization of more than 27,000 basic scientists and clinicians who study the brain and nervous system. The Society publishes The Journal of Neuroscience. To reach Schwarzschild, please call Georgia Pierce in the MGH public affairs office at 617-724-6423.
