Your gut health linked to Alzheimer’s disease, new study confirmed

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Alzheimer’s disease is the most common cause of dementia.

Still incurable, it directly affects nearly one million people in Europe, and indirectly millions of family members as well as society as a whole.

In recent years, the scientific community has suspected that gut microbiota plays a role in the development of the disease.

In a new study, researchers confirmed the link, in humans, between an imbalance in the gut microbiota and the development of amyloid plaques in the brain, which are at the origin of the neurodegenerative disorders characteristic of Alzheimer’s disease.

Proteins produced by certain intestinal bacteria, identified in the blood of patients, could indeed modify the interaction between the immune and the nervous systems and trigger the disease.

These results make it possible to develop new preventive strategies based on the modulation of the gut microbiota of people at risk.

The research was conducted by a team from the University of Geneva and elsewhere.

The team has been working for several years now on the potential influence of the gut microbiota on the brain, and more particularly on neurodegenerative diseases.

They have already shown that the gut microbiota composition in patients with Alzheimer’s disease was altered, compared to people who do not suffer from such disorders.

Furthermore, they have also discovered an association between an inflammatory phenomenon detected in the blood, certain intestinal bacteria and Alzheimer’s disease.

In the study, the hypothesis that the team wanted to test here: could inflammation in the blood be a mediator between the microbiota and the brain?.

They examined a group of 89 people between 65 and 85 years of age.

Some suffered from Alzheimer’s disease or other neurodegenerative diseases causing similar memory problems, while others did not have any memory problems.

Using PET imaging, they measured their amyloid deposition and then quantified the presence in their blood of various inflammation markers and proteins produced by intestinal bacteria, such as lipopolysaccharides and short-chain fatty acids.

The results are indisputable: certain bacterial products of the intestinal microbiota are linked to the quantity of amyloid plaques in the brain.

They found high blood levels of lipopolysaccharides and certain short-chain fatty acids (acetate and valerate) were linked to both large amyloid deposits in the brain.

Conversely, high levels of another short-chain fatty acid, butyrate, were linked to less amyloid pathology.

This work thus provides proof of an association between certain proteins of the gut microbiota and cerebral amyloidosis through a blood inflammatory phenomenon.

Scientists will now work to identify specific bacteria, or a group of bacteria, involved in this phenomenon.

This discovery paves the way for potentially highly innovative protective strategies—through the administration of a bacterial cocktail, for example, or of pre-biotics to feed the “good” bacteria in the intestine.

One author of the study is neurologist Giovanni Frisoni, the director of the HUG Memory Centre.

The study is published in the Journal of Alzheimer’s Disease.

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