Research conducted by scientists at the University of South Florida suggests that caffeine may help stop the production of the protein plaques that cause Alzheimer’s disease. The study was carried out on 55 mice, which had been bred specifically to develop symptoms of the disease. At the age of 18 to 19 months, the equivalent of 70 in human years, the mice underwent behavioral tests to first demonstrate that they indeed had memory impairments. Half of the mice were then given 500 milligrams of caffeine in their drinking water – the equivalent of drinking five cups of regular coffee a day. The other half received plain water.
Two months later, the researchers found that those mice that had caffeine performed much better on tests measuring their memory and thinking skills – in fact, as well as mice of the same age without dementia. Those who drank plain water continued to fare poorly on the same tests. Moreover, upon further examination, the brains of the mice given caffeine exhibited an almost 50 percent reduction in beta amyloid protein levels – the protein that forms destructive clumps in the brains of dementia patients. Through additional tests, the researchers found that caffeine affects the production of both enzymes required for the production of beta amyloid and that caffeine suppresses inflammatory changes in the brain that can result in the overproduction of the protein.
“The results are particularly exciting in that a reversal of pre-existing memory impairment is more difficult to achieve,” says Dr Gary Arendash, who led the study. “They provide evidence that caffeine could be a viable treatment for established Alzheimer’s disease and not simply a protective strategy. That’s important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process.” The team is hoping to begin human trials to determine if they can replicate their findings in people.
News Release: Coffee may reverse Alzheimer’s http://news.bbc.co.uk/2/hi/health/8132122.stm July 5, 2009
