Coffee drinkers who worry that their morning fix might not be the healthiest of habits may find comfort in a recent report. Working with a mouse model of Parkinson's disease, scientists at Massachusetts General Hospital (MGH) have shown that caffeine is able to prevent the loss of the chemical signal that is depleted in Parkinsons disease. Published in the May 15th Journal of Neuroscience, the study links caffeine's effects to the A2A receptor located on neural 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 dopaminergic neurons that go awry in Parkinson's disease. "The A2A receptor has a distinct advantage when it comes to treatment because it exists for the most part where you want to target your therapy. So there may be fewer side effects," says Michael A. Schwarzschild, MD, PhD, assistant professor of Neurology at MGH and principal investigator.
Caffeine acts as an antagonist to the A2A receptor, blocking its binding site and rendering it inactive. The scientists found that the effects of caffeine were mimicked by several known A2A antagonists as well as by genetic inactivation of the A2A receptor. The mouse study adds to epidemiological data published last year that documented how much coffee people drank and compared it to whether they developed Parkinsons. According to Schwarzschild, the results indicate that caffeine may be linked to a decreased risk of Parkinsons.
"Once this association was found, people asked if caffeine had an effect on the disease, or rather, does Parkinsons have an effect on caffeine consumption," says Jiang-Fan Chen, MD, PhD, assistant professor of Neurology at MGH and scientific co-director of the project. In other words, perhaps a brain destined to be affected by Parkinsons also is resistant to caffeine addiction.
Contact: Georgia W. Peirce
Massachusetts General Hospital