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
In contrast to the long-standing recognition of its dysfunction in Alzheimer's disease (AD), the exact role of CIV deficit in the pathogenesis of this neurodegenerative disorder remains poorly defined.
方法
Lastly, a proteome-wide association study (PWAS) using genetic data from large-scale AD cohorts identified that downregulation of COX11, a crucial CIV assembly factor, confers susceptibility to AD risk.
核心结论
In this study, by incorporating clinical resources, mouse- and human-based models of AD risk, and a genetic approach to bypass defective CIV via the ectopic expression of alternative oxidase (AOX), we examined whether CIV deficits are a pathogenic driver of…；Our results showed a clinicopathological association between neuronal CIV dysfunction and pathological characteristics of AD.；Collectively, our findings suggest that CIV dysfunction is a detrimental pathology contributing to AD-associated mitochondrial and neuronal damage.
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：把线粒体复合物 IV 损伤定位为 AD 易感的共同病理节点，为「线粒体功能 → 神经退行」提供遗传—功能双证据。 ｜ 价值分 1.7/5（★★☆☆☆）
全文来源
未取到全文 → 本卡为摘要级解读，未核验全文
原文题录
- 英文标题：Mitochondrial complex IV disruption is a detrimental pathology conferring ssusceptibility to alzheimer's disease.
- 期刊与标识：Molecular psychiatry · PMID 42963367 · DOI 10.1038/s41380-026-03935-3
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。