时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
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。
摘要（PubMed 原文节选）
Maintenance of protein homeostasis is essential for neuronal survival, and its disruption is a defining feature of neurodegenerative diseases. Neurons are particularly vulnerable to proteostatic stress due to their post-mitotic nature, long lifespan, and dependence on cytoskeletal integrity for structural stability, intracellular transport, and synaptic function. In tauopathies and related neurodegenerative disorders, misfolded proteins and aggregation-prone proteins burden the cellular quality-control systems, leading to cytoskeletal destabilization, synaptic dysfunction, and progressive neuronal loss. This review is organized around a central question: for a given tau species, defined by i…
对本项目的价值
中等价值：属「营养感知—自噬—蛋白稳态轴」方向；mTOR / 自噬 / 蛋白质稳态栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.2/5（★★☆☆☆）
全文不可及原因
无 PMCID 且 OpenAlex / Unpaywall 未提供可下载 OA PDF
原文题录
- 中文题名：神经退行中的蛋白质质量控制系统：分子伴侣、细胞骨架与 tau 的致病转变
- 英文标题：Protein Quality Control Systems in Neurodegeneration-Chaperones, Cytoskeleton, and the Pathogenic Transition of Tau.
- 期刊与标识：Mol Neurobiol · PMID 42965640 · DOI 10.1007/s12035-026-06310-z · EDAT 2026-10-31