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Caffeine May Fight Alzheimer’s Disease: Study

German and French researchers, in a collaborative study, found that caffeine positively impacts tau deposits in Alzheimer's disease. Tau deposits are an important characteristic features of the disease just like beta-amyloid plaques.

Vishakha Sonawane, HNGN, Apr 8, 2014

Researchers explained that these protein deposits hamper the communication between the nerve cells in the brain. This leads to degeneration of the nerve cells.  Researchers say caffeine is an adenosine receptor antagonist that stops various receptors in the brain activated by adenosine. It means that adenosine binds with the same receptors but does not block neural activity.

Past studies have shown that the barrier caused by the adenosine receptor subtype A2A in particular plays a chief role.

Dr Christa E Müller of the University of Bonn along with her colleagues developed an A2A antagonist in ultrapure and water-soluble form (designated MSX-3). They found that this particular compound leads to fewer harmful effects than caffeine as it is more effective in blocking only the A2A adenosine receptor subtype.

The study was conducted on mice treated with A2A antagonist. The control group were put on placebo. The results showed mice treated with A2A antagonist showed significantly better results on memory tests.

The researchers said that they found the A2A antagonist exhibited positive effects on spatial memory in particular. They also found that the treatment enhanced activity in the hippocampus, the part of the brain responsible for memory.

The findings are important as it might make way for the development of a new class of drugs that can help treat Alzheimer's disease. At present there are no drugs to cure the disease.

"We have taken a good step forward," said Müller in a press release. "The results of the study are truly promising, since we were able to show for the first time that A2A adenosine receptor antagonists actually have very positive effects in an animal model simulating hallmark characteristics and progression of the disease. And the adverse effects are minor."

Researchers said the next step is to test the A2A antagonist in additional animal and human models.

"Patience is required until A2A adenosine receptor antagonists are approved as new therapeutic agents for Alzheimer's disease. But I am optimistic that clinical studies will be performed," concluded Müller.

The findings are published in the journal Neurobiology of Aging.

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