PI3P：应对C9-ALS/FTD的（DPR）挑战。

IF 14.7 1区医学 Q1 NEUROSCIENCES

Neuron Pub Date : 2025-05-07 DOI:10.1016/j.neuron.2025.04.007

Janani Parameswaran, Zachary T McEachin

引用次数: 0

摘要

C9orf72中六核苷酸G4C2重复扩增导致二肽重复（DPR）蛋白积累，是肌萎缩侧索硬化症（ALS）和额颞叶痴呆（FTD）的主要遗传原因。在最近一期的Neuron杂志上，Zhang等人1报道了PI3P水平升高可减轻内溶酶体缺陷和dpr相关的神经毒性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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PI3P: Rising to the (DPR) challenge in C9-ALS/FTD.

A hexanucleotide G₄C₂ repeat expansion in C9orf72 causes accumulation of dipeptide repeat (DPR) proteins and is the leading genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In a recent issue of Neuron, Zhang et al.¹ report that elevating PI3P levels mitigates endolysosomal deficits and DPR-associated neurotoxicity.

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来源期刊

Neuron 医学-神经科学

CiteScore

24.50

自引率

3.10%

发文量

382

审稿时长

1 months

期刊介绍： Established as a highly influential journal in neuroscience, Neuron is widely relied upon in the field. The editors adopt interdisciplinary strategies, integrating biophysical, cellular, developmental, and molecular approaches alongside a systems approach to sensory, motor, and higher-order cognitive functions. Serving as a premier intellectual forum, Neuron holds a prominent position in the entire neuroscience community.