生物标志物 生物标志物
Marcel Seungsu Woo1, Joseph Therriault2, Yi-Ting Wang2
1University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 26, 2025
概括
神经炎症和细胞死亡途径驱动阿尔茨海默病 (AD) 的进展,即使在临床前阶段. 针对这些过程的早期干预对于管理AD至关重要.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 老年学是指老年学的学科.
背景情况:
- 神经炎症是阿尔茨海默病 (AD) 的关键特征,有助于粉样β (Aβ) 和神经纤维结 (NFT) 的积累.
- 神经炎症在临床前阿尔茨海默病进展中的具体作用尚不清楚.
研究的目的:
- 研究神经炎症在阿尔茨海默病 (AD) 在不同认知阶段的进展中的作用.
- 确定与神经炎症和AD进展相关的特定生物途径.
主要方法:
- 利用核酸链接免疫三明治测试 (NULISA) 针对不同参与者群体的向蛋白质组,包括认知不受损的个体,轻度认知障碍患者,AD患者和对照组.
- 使用无监督分析,横截面关联和纵向随访 (平均26个月) 用PET成像 (Aβ,tau),MRI和血液酸 (p-tau) 分析物.
主要成果:
- 脑脊液中细胞质激活,免疫信号和信号的签名随着年龄的增长和AD连续性而增加,在具有粉样蛋白阳性 (CU A+) 的认知不受损的个体中早期出现.
- 在CU参与者的纵向数据显示,神经炎症,质细胞激活,细胞死亡途径和线粒体运输缺陷增加,特别是在A+个体中,与p-tau217进展相关.
- 调解分析表明,细胞死亡途径和质细胞激活会调解早期AD进展 (p-tau217) 对神经炎症的影响,突触信号和线粒体运输会影响细胞死亡途径的激活.
结论:
- 神经炎症和细胞死亡途径是临床前和早期AD疾病进展的重要驱动因素.
- Aβ可能会触发神经炎症,质细胞激活和神经元功能障碍的循环,突出显示了对AD早期免疫调节干预的需要.
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