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

Abstract

Background 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. Method 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. Results 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. Conclusion 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.

Effects of ginseng on short‐chain fatty acids and intestinal microbiota in rats with spleen‐qi deficiency based on gas chromatography–mass spectrometry and 16s rRNA technology

“…31 Romboutsia was increased in the spleen-qi deficiency model group, and Romboutsia with high abundance was also found in the intestinal flora of Alzheimer's disease patients. 32,33 It can be concluded that the intestinal microbiota structure of rats with spleen-qi deficiency syndrome changes significantly, which affects intestinal metabolism and body immunity, and will promote the development of the disease.…”

Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases

“…299,300 Moreover, probiotic and prebiotic interventions aimed at elevating SCFA levels have demonstrated neuroprotective effects in AD mouse models by inhibiting glial activation and Aβ deposition. [301][302][303][304][305][306] Elevating butyrate through probiotic intervention (Clostridium butyricum) has been shown to inhibit microglial activation and reduce the levels of levels pro-inflammatory cytokines in APP/PS1 mice. Furthermore, butyrate exerts anti-inflammatory effects by downregulating the levels of cyclooxygenase-2 (COX-2) and CD11b, and suppressing NF-κB signaling in Aβ-induced BV-2 cells.…”