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
研究问题
Regarding whether MS leads to mitochondrial dysfunction, current research has not provided direct evidence that MS directly causes mitochondrial dysfunction.；These drugs aim to enhance mitochondrial function and antioxidant capacity by elevating intracellular NAD+ levels.；It remains incompletely resolved whether mitochondrial defects represent primary initiating triggers or predominantly secondary downstream consequences of protein aggregation, neuroinflammation or synaptic failure in sporadic neurodegeneration.
方法
In pathological conditions, ROS elevation exhibits quantitative differences among disease contexts.；44 Such quantitative heterogeneity reflects distinct upstream pathological triggers across different neurodegenerative disorders.；Consequently, antioxidant systems become both functionally impaired and quantitatively overwhelmed, establishing a feed‑forward oxidative‑stress vicious cycle within dopaminergic neurons.
核心结论
29 Collectively, these molecular defects lower oxidative‑phosphorylation efficiency, reduce cellular ATP supply and exacerbate electron leakage that fuels further ROS production.；Post‑mortem brain samples from AD and PD patients demonstrate significantly reduced enzymatic activity of SOD, CAT and GPx, which further impairs cellular ROS‑scavenging capacity and accelerates neuronal oxidative injury.；These changes collectively affect mitochondria, leading to a decline in their function and neuronal damage, ultimately triggering the occurrence and development of PD.
局限
Unlike dividing somatic cells, neurons cannot dilute damaged organelles via cell division.；41 However, mitochondrial function is not always flawless.
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；脑老化 / 神经退行 / 认知栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 135,679 字符，题名指纹 0.75，已过 DOI 逐字 + 题名指纹 + 正文长度三重归属校验）
原文题录
- 中文题名：神经退行的「隐形杀手」：线粒体功能障碍的机制、通路与治疗策略
- 英文标题：The "Invisible Killer" of Neurodegeneration: Mitochondrial Dysfunction in Neurodegenerative Disorders, Mechanisms, Emerging Pathways and Therapeutic Strategies.
- 期刊与标识：J Inflamm Res · PMID 42967168 · DOI 10.2147/JIR.S653025 · PMC PMC13723238 · EDAT 2026-11-01