阿克尔曼西亚尼菲拉囊泡通过ILA介导的AhR依赖的微质重编程减轻吸烟引起的认知衰退
Bowen Zhu1, Jiayuan Huang2, Haoran Zhang3
1Department of Anesthesiology, Shenzhen Hospital, Southern Medical University, Shenzhen, 518101, China.
Journal of nanobiotechnology
|January 24, 2026
概括
慢性吸烟通过改变肠道细菌,减少Akkermansia muciniphila (A. muciniphila) 和英多尔-3-乳酸 (ILA) 来损害认知能力. 补充A. muciniphila或ILA可以防止认知能力下降.
科学领域:
- 神经科学是一个神经科学.
- 微生物学 微生物学
- 胃肠病学 胃肠病学
背景情况:
- 慢性吸烟加快了与年龄相关的认知衰退.
- 连接吸烟与认知障碍的机制尚未完全理解.
- 肠道功能失调症越来越被认为是神经系统疾病的一个因素.
研究的目的:
- 阐明吸烟引起的肠道失调有助于认知障碍的途径.
- 调查Akkermansia muciniphila (A. muciniphila) 和其代谢物英多尔-3-乳酸 (ILA) 在吸烟相关认知缺陷中的作用.
- 确定预防吸烟者的认知衰退的潜在治疗点.
主要方法:
- 从暴露于烟雾的捐赠者移植便微生物群到接受者小鼠.
- 使用来自A. muciniphila的外膜囊泡 (OMV) 或外源性ILA.
- 认知功能,微质功能和突触完整性的评估.
- 对酸受体 (AhR) 信号通路和微质代谢的分析.
主要成果:
- 吸烟引起的肠道失调症,以减少A. muciniphila和ILA为特征,与认知缺陷相关.
- 来自暴露于烟雾的捐赠者的便微生物群在接受者小鼠中引起认知障碍和微质功能障碍.
- 用OMV或ILA治疗恢复了突触完整性并减轻了认知缺陷.
- OMV 和 ILA 激活 AhR 信号,重编程微质代谢以氧化酸化和减少神经炎症.
结论:
- 吸烟引起的肠道失调症,特别是减少的A. muciniphila和ILA,通过AhR信号传递促进认知障碍.
- A. muciniphila-ILA-AhR轴是缓解吸烟相关认知衰退的有希望的治疗标.
- 恢复肠道微生物代谢物可以防止神经炎症并恢复认知功能.
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