What do we know about caffeine and Alzheimer's?

By Annie Harrison-Dunn

- Last updated on GMT

There's still much to learn about the role of caffeine in the onset of Alzheimer's disease, say researchers
There's still much to learn about the role of caffeine in the onset of Alzheimer's disease, say researchers

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It is ‘imperative’ more research is conducted on the potential benefits of caffeine in the treatment and prevention of Alzheimer's disease, say scientists.

The researchers, of various disciplines from neurosurgery to psychiatry to family and community medicine, said: Based on the results from various studies, it is vital to focus on caffeine as a crucial part of the development of treatment and management of substances for Alzheimer's disease.”

Writing in the Journal of Caffeine Research​, they added: “It will also increase the number of studies and expand the knowledge base on the role of caffeine in relation to the pathology of Alzheimer's. It is therefore imperative for research to continue, geared toward investigating the potential use of caffeine in the treatment, prevention, and/or alteration of disease course for those affected by Alzheimer's.”

However, they warned this research must also look at the possible side effects of chronic caffeine consumption in this patient population such as stiffening of the arteries, increased levels of homocysteine, insulin and possibly cholesterol.

Alzheimer's disease is thought to be caused by protein misfolding and is a common cause of adult dementia following the accumulation of abnormally folded beta-amyloid (βA) plaques.

Research in mice suggested that caffeine helped slow down or prevent the development of βA plaques. They also pointed to evidence of caffeine’s ability to fight off age-related cognitive decline and improve symptoms of confusion. Human data was needed to confirm these results, they said.

Pinpointing the cause 

Scientists have looked to βA plaque accumulation as the disease’s primary cause, yet the mechanism around this was still unclear. Some had suggested other factors like the generation of antibodies which attacked the βA protein were key while other researchers questioned whether βA was the primary cause at all. 

βA is thought to be involved in neuronal development, but its function is not actually known.

Commenting on the paper, Professor Patricia Broderick, the journal’s editor-in-chief, said: “To say that strategizing medicines to treat Alzheimer's disorders is important is an understatement. Moreover, to say that caffeine is just an ordinary staple in our lives, whether caffeine is part of coffee or a chocolate bar, is also an understatement.”

The review was conducted by researchers from the Old Dominion University in Virginia, New York Medical College/Westchester Medical Centre, Baylor Medical College in Texas, Medical University of South Carolina, University of Virginia Health System, University of Toronto, University of Toledo Medical School in Ohio and the Eastern Virginia Medical School and the GZA St Vincentius Hospital in Antwerp.


Source: Journal of Caffeine Research

Published online ahead of print, doi:10.1089/jcr.2014.0027

“Caffeine as Treatment for Alzheimer's Disease: A Review”

Authors: A. Mohan, A. J. Roberto, A. Mohan, L. Liogier-Weyback, R. Guha, N. Ravishankar, C. Rebello, A. Kumar and R. Mohan

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1 comment

problematic paper

Posted by Henry Olders, MD, FRCPC,

Many of the statements made in the article do not give any references. The title indicates that caffeine is the focus, but a number of the studies which are referenced focused on coffee, not caffeine per se.

Coffee contains chlorogenic acid, which as pointed out in this article, inhibits glucose absorption. The beneficial effects of coffee may be due to this: less glucose absorption leads to lower insulin levels which in turn reduces insulin resistance, including insulin resistance in the brain. Thus, coffee may contribute to reversing the subgroup of Alzheimer's disease which is believed to be due to insulin resistance (Diabetes type 3, as some are calling it).

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