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在阿尔茨海默病模型中,MS4A6A/Ms4a6d缺乏破坏神经保护性微质功能并促进炎症

Hai-Shan Jiao¹, Yi-Jun Ge¹, Liang-Yu Huang²

¹Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, National Center for Neurological Disorders, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China.

Molecular neurodegeneration

|August 28, 2025

概括

在MS4A6A的基因变异影响阿尔茨海默病 (AD) 的风险. 通过增强粉样蛋白清除和减少AD患者的神经炎症,增强MS4A6A可能是一个新的治疗策略.

科学领域:

神经科学
遗传学
免疫学

背景情况:

阿尔茨海默病 (AD) 是最常见的痴呆症,遗传因素影响风险.
包括MS4A6A在内的与小质相关的基因与阿尔茨海默病的发生有关.
增加的MS4A6A水平及其与神经病理学的相关性表明在阿尔茨海默氏症中起作用,但潜在的机制仍未明确.

研究的目的:

研究MS4A6A基因多态与阿尔茨海默病 (AD) 风险之间的联系.
探索MS4A6A在AD发病过程中的功能作用,特别是关于微质功能和神经炎症.
评估在AD中调节MS4A6A的治疗潜力.

主要方法:

对734121名受试者进行全基因组关联分析,以确定与AD风险相关的MS4A6A多态.
人类队列中MS4A6A表达与脑脊液AD生物标志物的相关性分析.
使用显微镜,生物化学和行为评估生成和分析Ms4a6d缺陷的APP/PS1小鼠模型.

主要成果:

发现了与AD风险和脑脊液β-粉样蛋白水平变化的新型MS4A6A突变.
表明小鼠的 Ms4a6d 缺陷会损害微质细胞的粉样蛋白清除,增加斑块负担和突触损伤.
通过抑制微质细胞和星球细胞中的NF- kB信号传递,表明 Ms4a6d 缺乏会加剧神经炎症.

结论:

在阿尔茨海默病模型中,MS4a6d缺乏会损害神经保护并加剧神经炎症.
足够的 Ms4a6d 表达增强了微质粉样蛋白清除并抑制了炎症,这表明了治疗潜力.
阿尔茨海默病患者的MS4A6A升高可能是补偿性的;增强MS4A6A对阿尔茨海默病是一种有前途的治疗策略.

关键词:

阿尔茨海默病其他:微细胞没有.神经炎症

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