Longevity

Longevity Briefs: How Gut Bacteria May Affect Your Risk Of Alzheimer’s Disease

Posted on 16 November 2020

Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Scientists have suspected for some time that bacteria in the gut could be linked to the development of Alzheimer’s disease, as it appears to be related to the overabundance of certain strains of bacteria. Exactly how bacteria in the gut can contribute to the development of Alzheimer‘s is not known.

What did the researchers do: Researchers from Switzerland and Italy collaborated to test the hypothesis that gut bacteria could contribute to Alzheimer’s disease by promoting inflammation in the blood. They recruited 89 elderly individuals with cognitive performance ranging from normal to levels consistent with dementia. They measured the levels of gut microbe-associated products in their blood and the amount of amyloid plaque formation in their brains (amyloid plaque is highly associated with Alzheimer’s disease).

Key takeaway(s) from this research: Levels of certain bacterial products in the blood were associated with the amount of amyloid plaque in the brain. These products included short-chain fatty acids and lipopolysaccharide (LPS), a highly inflammatory component of some bacterial cell walls that have previously been found within amyloid plaques themselves. These bacterial products were also associated with higher levels of inflammatory molecules. This suggests that LPS and short-chain fatty acids may form a link between gut bacteria, the immune system, and Alzheimer’s disease.

This research paves the way for more research into potentially using probiotics or bacterial cocktails to protect against the development of Alzheimer’s.


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References

Short-Chain Fatty Acids and Lipopolysaccharide as Mediators Between Gut Dysbiosis and Amyloid Pathology in Alzheimer’s Disease: DOI: 10.3233/JAD-200306

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