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Two back to back mouse studies by American and Japanese scientists, due to be published in the Journal of Alzheimer’s Disease have found that caffeine may prevent and reverse memory impairment and cognitive function in transgenic mouse models of Alzheimer’s disease (AD).
Alzheimer’s disease is thought to affect up to half of Americans over the age of 85 and it has been estimated that this and other dementias lead to a tripling of health care costs for those over 65. Arendash et al first became interested in the ability of caffeine to treat AD when they read a previous Portuguese study which noted that people already with AD had consumed less caffeine over the previous 20 years than those without the disease. Several previous studies had also indicated caffeine might be capable of protecting memory, but these were not properly controlled clinical studies.
The researchers took 55 transgenic mice, genetically altered to develop symptoms of AD and conducted behavioural tests at the age of 18-19 months (equivalent to about 70 years in human terms) which showed symptoms of memory impairment. The mice were split into two groups, one receiving plain water to drink (the control) whilst the other group were given 500mg caffeine per day added to their drinking water, this being the equivalent of 5 cups of coffee or 14 cups of tea. After two months the mice were tested again and those in the caffeine group had improved performance and fared as well as normal mice of a similar age. The researchers discovered that those mice in the caffeine group had nearly 50% less beta-amyloid (the protein that forms sticky clumps in the brains of people with AD) in their brain compared to the control group.
In the other study by the same team, young and old transgenic AD mice were also given caffeine. The researchers discovered that this rapidly reduced the beta-amyloid levels in both the blood and the brain interstitial fluid. Long term caffeine treatment of old AD mice appeared to sustain reduction in blood beta-amyloid levels and also decreased soluble and deposited beta-amyloid in the brain.
It was also observed that feeding caffeine to normal mice did not boost their memory, which suggested that caffeine was not able to improve memory performance above normal levels. Arendash et al suggest that caffeine appears to reduce both of the enzymes required to produce beta-amyloid and that it may also inhibit inflammation which causes too much of the protein to be created. Dr Huntingdon Potter, director of the Florida Alzheimer’s Disease Research Centre where some of the research was performed is quoted in Medical News Today as saying that these are some of the most promising Alzheimer’s mouse experiments ever done. They show that caffeine rapidly reduced beta-amyloid protein in the blood and the brain and this reduction is linked to cognitive benefit. Dr Potter also noted that the researchers have already shown that giving caffeine to elderly people without dementia quickly affects their blood beta-amyloid levels, as happened for the mice. The scientists are now trying to obtain funding to see if these results could be replicated in human clinical trials. Arandash told the BBC that these results provided evidence that caffeine could be a viable treatment for established AD and not simply as a protective strategy. He added that this was important as caffeine is a safe drug for most people. (Science Daily).
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