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质细胞炎症和细胞死亡途径在临床前和早期AD中驱动疾病进展

Marcel S Woo^1,2,3, Joseph Therriault^4,5,6, Seyyed Ali Hosseini^4,5,6

¹Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, McConnell Brain Imaging Centre (BIC), Montreal Neurological Institute, Montréal, QC, Canada. m.woo@uke.de.

EMBO molecular medicine

|October 10, 2025

概括

神经炎症和细胞死亡途径是阿尔茨海默病 (AD) 进展的早期驱动因素,甚至在症状出现之前. 针对这些过程可能为AD提供新的治疗策略.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
生物标志物发现发现

背景情况:

阿尔茨海默病 (AD) 涉及粉样β (Aβ) 和神经纤维细胞 (NFT),导致质激活和神经退行.
在临床前和早期症状性AD期间神经炎症在神经元损伤和疾病进展中的确切作用尚未完全理解.

研究的目的:

通过疾病连续性识别与阿尔茨海默病进展相关的途径.
调查神经炎症和细胞死亡途径在早期AD病变发生过程中的作用.

主要方法:

综合多重免疫测试和 SomaScan 脑脊液 (CSF) 的蛋白质组.
在整个AD连续的个体中利用MRI和PET脑成像.
采用公正的集群和调解分析来识别关键的病理驱动因素.

主要成果:

质介导炎症,细胞死亡途径 (CDP) 和突触病理被确定为早期Aβ诱导的变化.
这些早期变化与临床前阿尔茨海默病的疾病进展相关.
发现CDPs的激活是早期症状AD炎症的关键驱动因素.

结论:

一个循环的质介导的神经炎症和神经元损伤的特征临床前AD.
这些发现凸显了AD早期神经炎症和细胞死亡途径的重要性.
已识别的途径为新的AD治疗方法提供了潜在的目标.

关键词:

阿尔茨海默氏症是阿尔茨海默氏症的疾病.生物标志物生物标志物细胞死亡细胞死亡质细胞炎症质细胞炎症蛋白质组学是指蛋白质组学.

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