Amelioration of Serum Aβ Levels and Cognitive Impairment in APPPS1 Transgenic Mice Following Symbiotic Administration

Alzheimer's disease (AD) is a neurodegenerative process responsible for almost 70% of all cases of dementia. The clinical signs consist in progressive and irreversible loss of memory, cognitive, and behavioral functions. The main histopathological hallmark is the accumulation of amyloid-ss (A ss) peptide fibrils in the brain. To date, the origin of A ss has not been determined. Recent studies have shown that the gut microbiota produces A ss, and dysbiotic states have been identified in AD patients and animal models of AD. Starting from the hypothesis that maintaining or restoring the microbiota's eubiosis is essential to control A ss's production and deposition in the brain, we used a mixture of probiotics and prebiotics (symbiotic) to treat APPPS1 male and female mice, an animal model of AD, from 2 to 8 months of age and evaluated their cognitive performances, mucus secretion, A beta serum concentration, and microbiota composition. The results showed that the treatment was able to prevent the memory deficits, the reduced mucus secretion, the increased A beta blood levels, and the imbalance in the gut microbiota found in APPPS1 mice. The present study demonstrates that the gut-brain axis plays a critical role in the genesis of cognitive impairment, and that modulation of the gut microbiota can ameliorate AD's symptomatology.