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Caffeine affects Alzheimer's-related protein formation, improves memory

Friday, April 25, 2014 by: David Gutierrez, staff writer
Tags: caffeine, Alzheimer''s disease, memory performance

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(NaturalNews) Caffeine may slow the development of Alzheimer's symptoms, according to a study conducted by researchers from the University of Bonn, Germany, and the University of Lille, France, and published in the journal Neurobiology of Aging.

The researchers hope that their research may some day lead to a caffeine-based drug for Alzheimer's disease. Their work was funded by 30,000 ($40,000) from the non-profit Alzheimer Forschung Initiative and 50,000 ($70,000) from the French Partner organization LECMA

The study focused on deposits of tau proteins in the brain, one of the two proteins (along with amyloid-beta) linked to the development of Alzheimer's disease. Researchers believe that these proteins disrupt neural communication and lead to brain cell death. This, in turn, produces the characteristic symptoms of the disease, such as memory loss, personality change and loss of ability to carry out daily tasks.

Prior studies have suggested that regular, moderate caffeine intake reduces the risk of developing Alzheimer's disease and prevents memory loss in the elderly. Caffeine has also been shown to slow memory loss in rats bred to develop amyloid-beta deposits in their brains. A 2011 study conducted by researchers from the University of South Florida found that caffeine somehow stimulates blood levels of a protein that slows the development of Alzheimer's.

Caffeine blocks key neurotransmitter

In a prior study, German and French researchers had found that a specific receptor for the neurotransmitter adenosine might play an important role in the loss of memory in mice bred to develop tau deposits. Because caffeine blocks adenosine receptors in the brain, the researchers suspected that this might underlie the chemical's Alzheimer's-fighting effects.

For the new study, the researchers modified caffeine into a water-soluble, ultrapure blocker specific to the adenosine receptor A2A. Because the caffeine chemical had been modified, it did not interfere with other adenosine receptors but was significantly more effective at blocking A2A. One group of tau-predisposed mice was given 0.3 g of this chemical per liter of drinking water, while another group was not given the chemical.

The researchers found that mice given the caffeine-related chemical performed significantly better on memory tests -- especially tests of spatial memory -- than mice in the control group. They also had less damage to the hippocampus, the brain structure believed to control memory in rodents.

"We have taken a good step forward," researcher Christa E. Muller said. "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."

If further animal tests support these findings, the new caffeine-based chemical could be tested on humans as a potential treatment for Alzheimer's disease.

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

Consume with caution

Although caffeine does appear to have certain health benefits, as demonstrated in the Alzheimer's study, excessive caffeine consumption can have serious negative health effects as well. Caffeine is addictive and can produce dependency and crippling withdrawal. It can also worsen or even produce anxiety and its related symptoms. Some health professionals warn that, by overstimulating the sympathetic nervous system, excessive caffeine can lead to adrenal fatigue.

Studies have also linked excessive caffeine consumption during pregnancy to higher rates of miscarriage and lower birth rates, and have suggested that it worsens blood sugar regulation in diabetics.

Sources for this article include:












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