Caffeine may aid the progression of Alzheimer's disease, according to a recent study.

A research team, led by Dr. Christa E. Müller from the University of Bonn and Dr. David Blum from the University of Lille, was able to demonstrate that caffeine has a positive effect on tau deposits in Alzheimer's disease. The findings could result in a new class of drugs being developed for the treatment of the disease.

Tau deposits, along with beta-amyloid plaques, are among the characteristic features of the degenerative brain disease. These deposits disrupt the communication of the nerve cells in the brain and contribute to their decline.

Researchers found that caffeine, an adenosine receptor antagonist, blocks various receptors in the brain which are activated by adenosine. Researchers had already established, based on initial results, that the blockade of the adenosine receptor subtype A2A in particular could play an important role in fighting against Alzheimer's.

Initially, researchers developed an A2A antagonist in ultrapure and water-soluble form. This compound had fewer adverse effects than caffeine since it only blocks only the A2A adenosine receptor subtype, and at the same time it is significantly more effective. Over several weeks, the researchers then treated genetically altered mice with the A2A antagonist. The mice had an altered tau protein which, without therapy, leads to the early development of Alzheimer's symptoms.

Researchers found that in comparison to a control group which only received a placebo, the treated animals achieved significantly better results on memory tests. The A2A antagonist displayed positive effects in particular on spatial memory.

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

The findings were recently published in the online edition of the journal Neurobiology of Aging.