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
研究问题
However, post-mortem tissue predominantly reflects advanced or terminal disease and cannot establish the temporal sequence of these abnormalities or determine whether mitochondrial dysfunction is an initiating event, a consequence of…；In vitro models therefore remain valuable for isolating the direct effects of defined αSyn species and investigating mitochondrial changes that may occur before overt cell loss.
方法
（原文未给出可直接抽取的对应表述）
核心结论
In contrast, oligomeric αSyn was more consistently associated with mitochondrial membrane depolarisation, increased ROS production, impaired respiration and ATP production, and activation of apoptotic pathways [ , , – , , , , , – ].；Treatment with A53T αSyn was also associated with enhanced cardiolipin binding and aggregation, alongside impaired complex I activity, increased mitochondrial ROS production, mitochondrial membrane permeabilisation and cell death [ ].；Compared with wild-type αSyn, treatment of cells with the A53T variant was associated with greater mitochondrial membrane disruption, nitric oxide release and S-nitrosylation, impaired mitochondrial quality control and increased apoptosis [ ].
局限
However, these effects were not uniform across cell models with evidence of different components of mitochondrial function impaired in response to αSyn, likely due to heterogeneity in experimental conditions.；Future studies comprehensively profiling metabolite concentrations in response to αSyn exposure may highlight pathways most affected and aid in identification of future therapeutic targets.
对本项目的价值
综述级证据，用于快速对齐领域共识与空白：神经退行是长寿干预最难攻的终点，本文提供机制或生物标志物层面的抓手。 ｜ 价值分 2.2/5（★★☆☆☆）
全文来源
PubMed PMC JATS 全文（正文 42,004 字符，已过 DOI 逐字 + 题名指纹双重归属校验）
原文题录
- 英文标题：Mitochondrial Dysfunction as a Convergent Mechanism of α-Synuclein Toxicity: A Systematic Review of In Vitro Fibrillar Models.
- 期刊与标识：Molecular neurobiology · PMID 42955574 · DOI 10.1007/s12035-026-06287-9
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