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铁可降低病理性α-突触核蛋白的传播:“脑铁蓄积可减轻原纤维注射后α-突触核蛋白的播散”一文的编辑要点,发表于第 554 页。

Iron reduces the propagation of pathological α-synuclein: An Editorial Highlight for "Brain iron enrichment attenuates α-synuclein spreading after injection of preformed fibrils" on page 554.

机构信息

Department of Neurology, State Key Laboratory of Biotherapy and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Sichuan, China.

West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Sichuan, China.

出版信息

J Neurochem. 2021 Nov;159(3):414-416. doi: 10.1111/jnc.15467. Epub 2021 Jul 23.

Abstract

Iron accumulation and α-synuclein aggregates (e.g., Lewy bodies) have been linked with the pathogenesis of Parkinson's disease (PD), with yet-to-be-determined interaction. Previous studies have indicated that iron binds to α-synuclein and triggers its aggregation in vitro, and iron is found enriched in Lewy bodies. In the current study, Joppe et al. have found that the propagation of pathological α-synuclein caused by intrastriatal α-synuclein preformed fibrils (PFFs) injection was unexpectedly attenuated in rodent brains in a model of brain iron elevation (neonatal iron feeding). PFFs stimulated microglial activation was also reduced in mice with elevated iron. These results may provide new insight into the complex interaction between these two key pathologies of PD.

摘要

铁积累和α-突触核蛋白聚集物(例如路易小体)与帕金森病(PD)的发病机制有关,但相互作用尚未确定。先前的研究表明,铁与α-突触核蛋白结合并在体外引发其聚集,并且铁在路易小体中富集。在目前的研究中,Joppe 等人发现,纹状体中α-突触核蛋白原纤维形成(PFFs)注射引起的病理性α-突触核蛋白的传播,在脑铁升高(新生铁喂养)的模型中出人意料地减弱。铁升高的小鼠中 PFFs 刺激的小胶质细胞激活也减少。这些结果可能为 PD 的这两种关键病理学之间的复杂相互作用提供新的见解。

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