C9orf72 ALS-FTD 神经元的毒性功能增益机制驱动自噬和溶酶体功能障碍

IF 14.6 1区生物学 Q1 CELL BIOLOGY

Autophagy Pub Date : 2024-04-14 DOI:10.1080/15548627.2024.2340415

Jimmy Beckers, Philip Van Damme

引用次数: 0

摘要

C9orf72基因的六核苷酸重复扩增是肌萎缩侧索硬化症（ALS）和额颞叶痴呆症（FTD）这两种相关神经退行性疾病的主要遗传原因。

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Toxic gain-of-function mechanisms in C9orf72 ALS-FTD neurons drive autophagy and lysosome dysfunction

Hexanucleotide repeat expansions in the C9orf72 gene are the primary genetic cause for both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative dise...

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来源期刊

Autophagy 生物-细胞生物学

CiteScore

21.30

自引率

2.30%

发文量

277

审稿时长

1 months

期刊介绍： Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.