Scientists working with a mouse model of Parkinson's disease have found that caffeine prevents the loss of the neurotransmitter dopamine, which is depleted in the neurodegenerative illness. If the new findings are any indication of caffeine's effects in humans, a coffee a day may help keep Parkinson's away. The results of this study will be published in the May 15 issue of the journal Neurology.

Specifically, the new research, conducted by Michael Schwarzchild of Massachusetts General Hospital and his colleagues, links caffeine's protective effects to the so-called A2A receptor. The dopamine neurons that degenerate in Parkinson's target neighboring neural cells that sport this receptor. But caffeine apparently antagonizes the A2A receptor, rendering it inactive and thereby halting the progressive destruction that characterizes the disease. Indeed, those mice in Schwarzchild's study that were pretreated with caffeine retained near-normal dopamine levels when exposed to a chemical known to induce Parkinson's-like symptoms by decreasing brain dopamine.

These findings follow on the heels of a study published last year, which found a link between caffeine consumption and a decreased risk of Parkinson's. At that time, some researchers suggested that rather than caffeine protecting against the disease, it might be that Parkinson's patients have a tendency to avoid addictive substances. The new results, however, show that caffeine can prevent the biochemical pattern of Parkinson's in mice. "The animal results lend more weight to caffeine's neuroprotective nature," Schwarzchild asserts. "But the results don't prove it, and they do not provide a rationale for changing coffee consumption habits." Thus, he says, it remains to be seen whether the mouse data will translate to humans.

Scientists working with a mouse model of Parkinson's disease have found that caffeine prevents the loss of the neurotransmitter dopamine, which is depleted in the neurodegenerative illness. If the new findings are any indication of caffeine's effects in humans, a coffee a day may help keep Parkinson's away. The results of this study will be published in the May 15 issue of the journal Neurology.

Specifically, the new research, conducted by Michael Schwarzchild of Massachusetts General Hospital and his colleagues, links caffeine's protective effects to the so-called A2A receptor. The dopamine neurons that degenerate in Parkinson's target neighboring neural cells that sport this receptor. But caffeine apparently antagonizes the A2A receptor, rendering it inactive and thereby halting the progressive destruction that characterizes the disease. Indeed, those mice in Schwarzchild's study that were pretreated with caffeine retained near-normal dopamine levels when exposed to a chemical known to induce Parkinson's-like symptoms by decreasing brain dopamine.

These findings follow on the heels of a study published last year, which found a link between caffeine consumption and a decreased risk of Parkinson's. At that time, some researchers suggested that rather than caffeine protecting against the disease, it might be that Parkinson's patients have a tendency to avoid addictive substances. The new results, however, show that caffeine can prevent the biochemical pattern of Parkinson's in mice. "The animal results lend more weight to caffeine's neuroprotective nature," Schwarzchild asserts. "But the results don't prove it, and they do not provide a rationale for changing coffee consumption habits." Thus, he says, it remains to be seen whether the mouse data will translate to humans.