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阿尔法同核素共同病理与阿尔茨海默氏症疾病中粉样蛋白驱动的加速积有关

Nicolai Franzmeier^1,2,3, Sebastian Niclas Roemer-Cassiano^4,5, Alexander Maximilian Bernhardt^5,6

¹Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany. nicolai.franzmeier@med.uni-muenchen.de.

Molecular neurodegeneration

|March 18, 2025

概括

阿尔法-同核素 (αSyn) 共同病理加速阿尔茨海默病 (AD) 的进展,通过恶化tau聚合和认知衰退. 使用基于CSF的种子放大试验 (SAA) 检测αSyn可以识别患有更晚期疾病的个体.

科学领域:

神经科学是一个神经科学.
神经病理学神经病理学
生物标志物发现发现

背景情况:

聚合的α-synuclein (αSyn) 是帕金森病的关键病理,也是阿尔茨海默病 (AD) 的常见共同病理.
临床前数据表明αSyn加剧tau聚合,可能导致AD的神经退行.
研究αSyn在阿尔茨海默病中的作用需要方法来检测它与粉样蛋白和蛋白病理一起的共同病理.

研究的目的:

为了确定αSyn共同病理是否加速粉样β (Aβ) 驱动的积和AD的认知衰退.
利用一种基于CSF的新型种子放大试验 (SAA) 在体内检测αSyn聚合.
使用PET成像,将αSyn阳性与tau生物标志物和认知轨迹相关联.

主要方法:

用于284名Aβ阳性和308名Aβ阴性个体的amyloid-PET,Flortaucipir tau-PET和CSF αSyn SAA.
脊髓的p-tau181水平和纵向的tau-PET (大约. 2.5年) 进行了分析.
线性回归模型评估了αSynSAA阳性,tau生物标志物和认知衰退之间的联系.

主要成果:

αSynSAA阳性在Aβ阳性个体中更常见,并且随着临床严重程度的增加而增加.
在AD典型区域,αSyn阳性与较高的粉样蛋白相关的CSFp-tau181和tau-PET水平相关.
纵向分析显示,αSyn阳性与更快的粉样蛋白相关的积和认知衰退有关.

结论:

通过CSF-SAA检测到的αSyn共同病理在晚期AD中很普遍,并加速认知衰退.
αSyn共同病理加剧了AD中粉样驱动的tau病理生理学.
针对αSyn可能对AD研究和治疗策略至关重要.

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