The more coffee people drink, according to some recent studies, the less likely they are to get Parkinson's disease. Now, researchers have shown in mice how caffeine may prevent the loss of dopamine, the critical brain chemical that is depleted by the disease. But they warn we're still a long way from prescribing double lattes to ward off Parkinson's.
Last year, the results of a 30-year study from Honolulu showed a strong inverse relationship between caffeine consumption and Parkinson's in 8000 men, backing up earlier epidemiological observations. And converging lines of evidence suggested that caffeine interacts with receptors known to congregate in one of the brain regions damaged by Parkinson's disease.
To examine the connection, a team led by Michael Schwarzschild and Jiang-Fan Chen of Massachusetts General Hospital in Boston, Massachusetts, made Parkinson's-like lesions by injecting a neurotoxin called MPTP into the brains of mice. In a week, dopamine levels in the area dropped by 85%. But if the mice were injected with a low dose of caffeine--equivalent to one or two cups of coffee in a human--prior to the MPTP hit, dopamine levels fell by only 60%, they report in the 15 May issue of the Journal of Neuroscience. At higher caffeine doses, MPTP toxicity could be completely prevented under some conditions. The researchers found that caffeine apparently blocks the A2A adenosine receptor, which occurs almost exclusively on neurons in the striatum, an area targeted by the disease. But it's not clear how the stifling of this receptor protects neurons.
"The results in the animal model complement quite nicely what we observed in humans," says Harvard University epidemiologist Alberto Ascherio, author of another recent study showing that the more coffee people drink, the less likely they are to develop Parkinson's. He emphasizes that none of the research proves a causal association between caffeine and risk of Parkinson's; nonetheless the "evidence is strong [that] caffeine may indeed prevent the disease."
Schwarzschild says the research raises the possibility that new drugs targeted at A2A receptors--which are currently in clinical trials--may not only relieve symptoms but actually retard the progress of the disease. But he emphasizes that "for now the findings provide no rational basis for changing one's caffeine intake."