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Drinking coffee could combat Alzheimer's disease, according to a new study.

Scientists from Germany and France found that caffeine has a positive effect on tau deposits in Alzheimer's disease.

Like beta-amyloid plaques, tau deposits one of the key features of Alzheimer's disease. Researchers said that these protein deposits disrupts the communication of the nerve cells in the brain that contribute to their degeneration.

Researchers said that latest findings could pave to way for the development of a new class of drugs that can help treat Alzheimer's disease. There are currently no drugs that can prevent the neurodegenerative disorder.

Researchers said that caffeine is an adenosine receptor antagonist that blocks various receptors in the brain that are activated by adenosine. Previous findings revealed that the blockade of the adenosine receptor subtype A2A in particular could play an important role. Müller and her team developed an A2A antagonist in ultrapure and water-soluble form (designated MSX-3). Researchers found that this compound had fewer adverse effects than caffeine is significantly more effective and because it only blocks the A2A adenosine receptor subtype. Researchers found that genetically altered mice that did not receive the A2A antagonist developed early signs of Alzheimer's disease. However, the treated mice achieved significantly better results on memory tests. Researchers found that the A2A antagonist displayed positive effects in particular on spatial memory. The study also found that the treatment also boosted activity in the hippocampus, the part of the brain responsible for memory.

"We have taken a good step forward," said Müller. "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.