Lv Xinhuang, Zhan Lu, Ye Tao, Xie Huijia, Chen Zhibo, Lin Yan, Cai Xianlei, Yang Wenwen, Liao Xiaolan, Liu Jiaming, Sun Jing
Department of Geriatrics, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, Zhejiang, China.
Department of Preventive Medicine, School of Public Health, Wenzhou Medical University, Wenzhou 325027, Zhejiang, China.
iScience. 2024 Oct 5;27(11):111116. doi: 10.1016/j.isci.2024.111116. eCollection 2024 Nov 15.
Gut microbiota plays a crucial role in the pathogenesis of Alzheimer disease (AD). Here, we found that AD patients had significantly lower abundance of , which were negatively correlated with cognitive impairment. Animal experiments showed that supplementation increased beneficial commensal bacteria, significantly improved pathological damage, and suppressed microglial activation in APP/PS1 mice. We further demonstrated that butyric acid, a metabolite of , reduced microglial activation and pro-inflammatory factor production via Akt/ nuclear factor κB (NF-κB) signal pathway . Meanwhile, we revealed that effectively inhibited activation of microglia in the APP/PS1 mice by regulating Akt/ NF-κB pathway. This finding highlights the role of and its metabolite butyrate in mitigating neuroinflammation in AD by modulating the Akt/NF-κB pathway.
肠道微生物群在阿尔茨海默病（AD）的发病机制中起着关键作用。在此，我们发现AD患者体内[具体细菌名称未给出]的丰度显著降低，且这些细菌与认知障碍呈负相关。动物实验表明，补充[具体细菌名称未给出]可增加有益共生菌，显著改善病理损伤，并抑制APP/PS1小鼠的小胶质细胞激活。我们进一步证明，[具体细菌名称未给出]的代谢产物丁酸通过Akt/核因子κB（NF-κB）信号通路减少小胶质细胞激活和促炎因子产生。同时，我们发现[具体细菌名称未给出]通过调节Akt/NF-κB通路有效抑制APP/PS1小鼠小胶质细胞的激活。这一发现突出了[具体细菌名称未给出]及其代谢产物丁酸盐通过调节Akt/NF-κB通路减轻AD神经炎症的作用。
