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We now know why coffee helps to stave off Alzheimer's disease

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Scientists recently discovered that caffeine consumption can be tied to a reduced risk of Alzheimer's disease and other neurodegenerative disorders. They knew that it was suppressing the rise of amyloid plaques in the brain, but why coffee consumption did the trick remained a mystery. But now, researchers from the University of Illinois believe they have found the answer, and it has to do with caffeine's ability to block inflammation in the brain — a discovery that could lead to new drugs which can prevent — or even reverse — mild cognitive impairment.

Hypoxic mice on caffeine

The study, which appears the Journal of Neuroscience, was conducted by Gregory Freund, a professor at U of I's College of Medicine. To reach his conclusion, Freund conducted an experiment on two groups of mice — one that was administered caffeine, and one that was not. Then, in order to facilitate cognitive impairment, he interrupted the breathing and blood flow of the mice (what's called hypoxia). He gave the mice a chance to recover, and then measured their ability to form new memories.


What Freund discovered was that, of the mice who consumed caffeine, they recovered their ability to form a new memory 33% faster than those mice who did not get the caffeine. This was a particularly pronounced effect — one that matched the anti-inflammatory impact of blocking IL-1 signalling — what has been implicated in the inflammation associated with Alzheimer's disease.

Blocking adenosine receptors

To better understand how caffeine was actually helping to reduce this inflammation, Freund considered the nature of the brain damage itself. What he discovered was that hypoxia kickstarts a complicated chain reaction that ends in cognitive decline. Caffeine, it now appears, minimizes the impacts of this chain reaction.


Hypoxia releases adenosine onto brain cells — and this is not good; adenosine molecules are what makes up ATP — the fuel that powers brain cells. What's essentially happening by virtue of the hypoxia is that this fuel is leaking all over the place — what Freund compares to highly volatile gasoline leaking out of a tank and threatening everything in its immediate surroundings.

This leaked adenosine triggers the activation of the caspase-1 enzyme, which in turn sets off the production of beta cytokine IL-1 — what is known to be a major player in inflammation.

But as Freund's study revealed, this cascade of despair is lessened by caffeine's ability to block adenosine receptors. In turn, this results in the brain's ability to stave of inflammation when confronted with either hypoxic effects or neurodegenerative disorders like Alzheimer's.

The entire study can be read at the Journal of Neuroscience.