A recent study conducted in 2020 by Italian and Swiss scientists and published in the Journal of Alzheimer Disease, confirmed metagenomic data supporting an association between certain intestinal bacterial strains and Alzheimer’s disease (AD). The study also uncovered association between amyloid pathology and gastrointestinal health using markers such as bacterial products like lipopolysaccharide (LPS), but also short-chain fatty acids (SCFAs: acetate, valerate, butyrate), inflammatory mediators, and markers of endothelial dysfunction in AD.

Eighty-nine individuals with cognitive performance ranging from normal to dementia were studied. Amyloid standardized uptake value ratio (SUVR) was positively associated with blood LPS (rho≥0.32, p≤0.006), acetate and valerate (rho≥0.45, p < 0.001), pro-inflammatory cytokines (rho≥0.25, p≤0.012), and biomarkers of endothelial dysfunction (rho≥0.25, p≤0.042). In contrast, it was negatively correlated with butyrate (rho≤–0.42, p≤0.020) and the anti-inflammatory cytokine IL10 (rho≤–0.26, p≤0.009). Endothelial dysfunction was positively associated with pro-inflammatory cytokines, acetate and valerate (rho≥0.25, p≤0.045) and negatively with butyrate and IL10 levels (rho≤–0.25, p≤0.038). The authors suggest a novel association between gut microbiota-related by-product and systemic inflammation with brain amyloidosis via endothelial dysfunction, suggesting that some SCFAs and LPS represent candidate pathophysiologic links between the gut microbiota and AD pathology. Probiotic supplementation, that still needs to be specifically formulated, is considered as a possible prevention in early stages of the AD’s neurodegenerative process.