College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City, China.
Institute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
CNS Neurosci Ther. 2023 Jun;29(6):1690-1704. doi: 10.1111/cns.14132. Epub 2023 Mar 8.
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.
肠道菌群被证明与阿尔茨海默病（AD）的进展有关，β-葡聚糖可以改善肠道菌群，β-葡聚糖是一种来源于酿酒酵母的多糖，通过肠道菌群影响认知功能。然而，β-葡聚糖对 AD 的影响是否参与其中尚不清楚。
本研究采用行为测试来测量认知功能。之后，采用高通量 16S rRNA 基因测序和 GC-MS 分析 AD 模型小鼠的肠道微生物群和代谢物 SCFAs，并进一步探索肠道菌群与神经炎症之间的关系。最后，采用 Western blot 和 Elisa 方法检测小鼠大脑中炎症因子的表达。
我们发现，在 AD 进展过程中适当补充 β-葡聚糖可以改善认知障碍和减少 Aβ斑块沉积。此外，补充 β-葡聚糖还可以促进肠道菌群组成的变化，从而改变肠道内容物中的菌群代谢物，并通过脑-肠轴减少大脑皮质和海马体中炎症因子和小胶质细胞的激活。同时降低海马体和大脑皮质中炎症因子的表达，从而控制神经炎症。
肠道微生物群和代谢物的失衡在 AD 的进展中起作用；β-葡聚糖通过改善肠道微生物群及其代谢物和减少神经炎症来阻止 AD 的发展。β-葡聚糖通过重塑肠道微生物群及其代谢物改善来治疗 AD 是一种潜在的策略。
