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在2型糖尿病中,大脑-肠道和微生物群-肠道-大脑通信与阿尔茨海默病有关

Yomna S Momen¹, Jayshree Mishra¹, Narendra Kumar¹

¹Department of Pharmaceutical Sciences, ILR College of Pharmacy, Texas A&M Health Science Center, Kingsville, TX 78363, USA.

|August 10, 2024

概括

饮食和2型糖尿病影响肠-大脑通信,影响阿尔茨海默病 (AD) 风险. 了解这些联系可能会揭示认知衰退的新治疗点.

科学领域:

神经科学是一个神经科学.
胃肠病学胃肠病学
微生物学微生物学

背景情况:

肠道微生物组通过肠-大脑轴通信显著影响健康.
阿尔茨海默病 (AD) 是一种进展性痴呆症,有多因素的原因,包括饮食和2型糖尿病 (T2D) 等可修改因素.
肠道功能失调和相关的炎症与T2D和AD病原发生有关.

研究的目的:

审查可修改因素,特别是饮食和T2D在微生物群-肠-大脑 (MGB) 和脑-肠 (BG) 通信中的作用.
阐明饮食影响肠道微生物群及其产物在T2D和AD中的机制.
根据MGB和BG的相互作用,探索阻碍AD进展的潜在治疗点.

主要方法:

文献综述侧重于饮食,肠道微生物群,T2D和神经健康之间的相互作用.
分析将高脂肪饮食 (HFD) 与肠道失调,炎症和认知障碍联系起来的机制性途径.
检查共享的分子通路,如转录因子和氨酸激酶表达,在肠-大脑通信.

主要成果:

由HFD引起的肠道失调促进了肠道屏障功能障碍和慢性低度炎症,导致肥胖和T2D.
肥胖和T2D与神经炎症,粉样β沉积和认知衰退有关,反映了HFD的影响.
饮食通过共享途径影响MGB和BG的沟通,可能会增加肥胖糖尿病患者的AD风险.

结论:

饮食和T2D显著调节肠道微生物群,影响MGB和BG的通信通路.
了解这些复杂的相互作用为认知障碍和AD的病变产生提供了洞察力.
识别共同的分子参与者为开发针对AD的新药学策略提供了基础.

关键词:

亚努斯酶是亚努斯酶的一种.肠-大脑轴肠-大脑轴肠道失生症 - - 肠道失生症益生菌益生菌益生菌益生菌是一种益生菌.交易监管交易监管交易监管交易监管

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