Alzheimer’s: how the gut makes us lose our head

Actu GP : Alzheimer : comment notre intestin nous fait perdre la tête

The link between an imbalance of the gut microbiota and Alzheimer’s disease has been confirmed. This study clarifies the mechanisms involved by identifying two weak links: inflammation and the barrier functions of the gut and brain.

 

A mind-boggling number of studies are published each month on the gut microbiota’s influence on brain function. Many of these studies focus on the role of gut microbiota imbalances in the onset or progression of Alzheimer’s disease (AD). The researchers in this study sought to identify the ways in which gut bacteria contribute to the disease, and more specifically to the accumulation of the dreaded amyloid deposits.

Uncovering the mechanisms at play in the gut-brain axis

To this end, they brought together around 90 individuals aged between 50 and 85, with or without AD, in order to study how the gut influences the brain. Analyses assessed the presence in their blood of: 1. molecules produced by bacteria from the gut microbiota; 2. inflammatory molecules; and 3. markers signaling the alteration of the gut barrier (allowing gut compounds to reach the bloodstream) and blood-brain barrier (allowing compounds to cross from the blood to the brain). The presence of amyloid deposits in the brain was also measured. The aim was to find associations between all these parameters in order to identify the mechanisms involved.

Bacterial and inflammatory compounds implicated

This search proved fruitful, with many strong associations found. For example, between amyloid deposits on the one hand and inflammation and presence in the blood of compounds from the gut microbiota on the other, or between these compounds and alterations to the permeability of the aforementioned barriers. An imbalance in the gut microbiota could therefore trigger an inflammatory mechanism capable of disrupting the body’s protective barriers, leading to the leakage of compounds into the brain and the potential formation of amyloid plaques. This finding opens the way to novel therapeutic approaches, such as the administration of a cocktail of beneficial bacteria (probiotics) to preserve the balance in the microbiota, particularly in at-risk individuals. The ingredients of this cocktail remain to be identified, however.

 

Sources:

Marizzoni M, Cattaneo A, Mirabelli P, et al. Short-Chain Fatty Acids and Lipopolysaccharide as Mediators Between Gut Dysbiosis and Amyloid Pathology in Alzheimer's Disease. J Alzheimers Dis. 2020;78(2):683-697