Caffeine may have positive effects on Alzheimer’s-related tau deposits, says study

By Anna Bonar

- Last updated on GMT

"Animals given caffeine achieved significantly better results on memory tests," said the researchers.
"Animals given caffeine achieved significantly better results on memory tests," said the researchers.

Related tags Alzheimer’s disease Caffeine

Caffeine could help ease the cognitive decline of Alzheimer’s disease German-French research has shown.

Tau protein deposits found in the brains of those suffering Alzheimer’s disease were crucial in cognitive decline as they could disrupt the communication of the brain’s nerve cells and thus lead to their degeneration.

The research published in the Neurobiology of Ageing​ journal studied the effects of caffeine administered at 0.3 g/L through drinking water on mice between 2-12 months of age. The researchers treated mice so that they had an altered tau protein that could lead to development of Alzheimer’s symptoms.

Memory tests

“In comparison to a control group which only received a placebo, the treated animals achieved significantly better results on memory tests,”​ said the researchers.

They found that chronic caffeine intake prevented the development of special memory deficits in tau mice through the Morris Water Maze test.

Moreover caffeine treatment eased some pro-inflammatory and oxidative stress markers. Stress was regarded as one of the reasons for the intensification of Alzheimer’s disease symptoms.

A step forward

"We have taken a good step forward. 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," ​said professor Christa Müller from the University of Bonn.

Source : 

Neurobiology of Ageing

Published online ahead of print DOI: 10.1016/j.neurobiolaging.2014.03.027

Beneficial effects of caffeine in a transgenic model of Alzheimer's disease-like tau pathology

Authors: C. Muller, D.Blum et al.

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