研究进展

脑脊液 p62/SQSTM1 与 tau 病理、脑结构改变及认知损害相关

来源:Journal of Alzheimer's disease : JAD · PMID 42961137 · DOI 10.1177/13872877261502791 · 来源:IMA 知识库《文献层·文献监控卡片》2026-11-01 期 · 摘要级(file_id dlMXdlgtPZzo,实际下载核验) · 摘要级,未获取付费墙全文

时间标签:数据日期 2026-11-01 · 生成时间 2026-11-01 05:30(Asia/Shanghai)| 检索窗口 PubMed edat 2026/10/31–2026/11/01 | 情报发生日期 2026-11-01

证据级别:摘要级。本条依据 PubMed 结构化摘要与元数据撰写,付费墙全文未获取、未逐节核验,本站未做任何数值推算补全。

研究问题

Multivariate regression and interaction analyses examined associations of CSF p62/SQSTM1 with cognition, AD biomarkers, and brain volumes and their modification by age, sex, APOE genotype, and diagnostic status.

方法

Longitudinal analyses further showed that participants in the highest quartile (Q4) exhibited an increased risk compared to the lowest (Q1) (HR = 1.78, 95% CI 1.16-2.73).

核心结论

Mediation analysis tested whether AD pathology and brain structure mediated the association between p62/SQSTM1 and cognition.ResultsElevated CSF p62/SQSTM1 levels correlated with poorer cognition, heightened tau pathology, increased sTREM2 and PGRN levels,…;Longitudinal analyses further showed that participants in the highest quartile (Q4) exhibited an increased risk compared to the lowest (Q1) (HR = 1.78, 95% CI 1.16-2.73).;Mediation analysis indicated that tau pathology and reduced brain volumes mediated the association between p62/SQSTM1 and cognition.ConclusionsHigher p62/SQSTM1 levels were associated with tau pathology and an elevated risk of AD.

局限

(原文未给出可直接抽取的对应表述)

对本项目的价值

高价值:脑脊液 p62/SQSTM1(自噬底物受体)与 tau 病理、脑结构改变和认知损害相关联 —— 自噬功能有了可进入人体研究的 CSF 读数。 | 价值分 1.2/5(★☆☆☆☆)

全文来源

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原文题录

  • 英文标题:Cerebrospinal fluid p62/SQSTM1 is associated with tau pathology, brain structural alterations, and cognitive impairment in adults without dementia.
  • 期刊与标识:Journal of Alzheimer's disease : JAD · PMID 42961137 · DOI 10.1177/13872877261502791

A 级证据分级:A 级(同行评议人体研究)

本文属人体研究证据,但需注意:观察性或小样本干预的结论不等于已证实临床获益;效应量与长期安全性仍需更大规模、更长随访的试验验证。

关于本文的文献来源:本站依据 IMA 知识库「五刊监控·深度文献卡片」(SOP §4.2 摘要级)撰写,依据期刊公开摘要与 PubMed 元数据;付费墙全文未获取之处已标注「待补全文」,未做任何数值推算补全。