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错误折叠的α-synuclein与阿尔茨海默病蛋白质病变的同时发生

Erin M Jonaitis^1,2,3, Karen MacLeod⁴, Jennifer Lamoureux⁴

¹Wisconsin Alzheimer's Institute, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association

|May 13, 2025

概括

在脑脊液中检测到错误折叠的α-synuclein (syn) 聚合物,与阿尔茨海默病标志物和认知衰退同时发生. 这表明在痴呆症风险队列中,综合病理是常见的.

科学领域:

神经科学是一个神经科学.
生物标志物发现发现
痴呆症研究痴呆症研究

背景情况:

多病因痴呆症需要体内共病理标志物.
错误折叠的α-synuclein (syn) 是一种关键蛋白质,与各种神经退行性疾病有关.
准确检测合成聚合物对于了解疾病机制至关重要.

研究的目的:

用种子放大试验 (synSAA) 测量脑脊液 (CSF) 中错误折叠的合成聚合物 (syn-seeds).
研究合成种子与已确定的阿尔茨海默病 (AD) 生物标志物之间的关系,包括酸化 (T) 和粉样β (A).
检查合成种子与认知状态和纵向认知衰退的关联.

主要方法:

在AD风险队列中的420名参与者的CSF样本使用synSAA.被分析.
将SynSAA结果与酸化 (T) 和粉样β (A) 的水平进行了比较.
用混合效应模型评估和建模了纵向认知表现.

主要成果:

合成阳性 (synSAA+) 与酸化阳性 (36%对20%,p=0.011) 有意义地相关.
synSAA+个体的认知障碍患病率较高 (10%与0%的痴呆症相比,p=0.00050).
与synSAA-参与者相比,synSAA+参与者的认知表现在数字符号替换测试中下降约40%更快.

结论:

这些发现支持阿尔法-同核素共病理在阿尔茨海默病风险队列中的存在,其中许多人没有认知障碍.
同核素阳性与阿尔茨海默病生物标志物和认知障碍有关.
需要进一步评估,以了解同核素和认知进展之间的关系,因为越来越多的参与者发展认知衰退.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.莱维体痴呆症 (Lewy体痴呆症) 是一种疾病.氨基化物氨基化物大脑脊髓液中的脑脊液.种子放大试验试验知道的知道的知道的

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