β-Glucan attenuates cognitive impairment of APP/PS1 mice via regulating intestinal flora and its metabolites.

Abstract

The intestinal flora has been shown to be involved in the progression of Alzheimer's disease (AD) and can be improved by β-glucan, a polysaccharide derived from Saccharomyces cerevisiae, which affects cognitive function through the intestinal flora. However, it is not known if this effect of β-glucan is involved in AD. This study used behavioral testing to measure cognitive function. After that, high-throughput 16 S rRNA gene sequencing and GC-MS were used to analyze the intestinal microbiota and metabolite SCFAs of AD model mice, and further explore the relationship between intestinal flora and neuroinflammation. Finally, the expressions of inflammatory factors in the mouse brain were detected by Western blot and Elisa methods. We found that appropriate supplementation of β-glucan during the progression of AD can improve cognitive impairment and reduce A β plaque deposition. In addition, supplementation of β-glucan can also promote changes in the composition of the intestinal flora, thereby changing the flora metabolites in the intestinal content and reduce the activation of inflammatory factors and microglia in the cerebral cortex and hippocampus through the brain-gut axis. While reducing the expression of inflammatory factors in the hippocampus and cerebral cortex, thereby controlling neuroinflammation. The imbalance of the gut microbiota and metabolites plays a role in the progression of AD; β-glucan blocks the development of AD by improving the gut microbiota and its metabolites and reducing neuroinflammation. β-Glucan is a potential strategy for the treatment of AD by reshaping the gut microbiota and improving its metabolites.