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后生物和肠-大脑轴:对调节神经炎症和认知衰老的机制性审查

Rijhul Lahariya¹, Gargee Anand², Bandana Kumari³

¹All India Institute of Medical Sciences, Patna, Bihar, India, 801507.

Journal of neuroimmunology

|January 22, 2026

概括

衰老会破坏肠-大脑轴,增加神经退行风险. 来自有益微生物的后生物,通过调节肠道健康和减少炎症来保护大脑,显示出有希望.

科学领域:

神经科学是一个神经科学.
微生物学微生物学
老年学是一门学科.

背景情况:

衰老导致肠道失调,影响肠-大脑轴 (GBA) 并促进神经炎症.
在老年人中,微生物多样性的减少和病原生物的增加会增加神经毒性代谢物,从而导致神经退行.
来自共生动物的神经保护性代谢物抵消这些影响,保持肠道完整性并增强神经元功能.

研究的目的:

为了合成连接肠道失调,代谢物和大脑衰老的机制.
评估后生物药物作为与年龄相关的神经退行相关的潜在精密疗法.
突出挑战和未来的方向,以翻译临床前发现人类临床应用.

主要方法:

审查临床前动物研究和人类翻译挑战.
分析涉及代谢物信号通路的分子机制 (例如,HDAC抑制,GPR信号).
综合多omics数据和临床试验的局限性.

主要成果:

老龄化中的肠道功能失调会增加神经毒性代谢物 (LPS,TMAO),并导致"炎症"和神经退行.
神经保护性代谢物 (SCFA,IPA) 支持肠道完整性和神经元的弹性.
在临床前模型中,后生菌显示出调节GBA,阻断LPS和增强神经元弹性.

结论:

后生物学为与年龄相关的GBA功能障碍和神经退行症提供了一个有希望的,精确的治疗策略.
克服人类转化方面的挑战,包括微生物群的变异性和标准化,至关重要.
多omics分层临床试验对于验证后生菌对认知健康和神经保护的疗效至关重要.

关键词:

认知老龄化认知老龄化肠-大脑轴肠-大脑轴微生物群中的微生物群神经退行性疾病是一种神经退行性疾病.神经炎症是一种神经炎症.后生物学的后生物学.

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