期刊
NEUROSCIENCE LETTERS
卷 636, 期 -, 页码 3-8出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2016.04.065
关键词
ALS; SOD1; FUS/TLS; TDP43; Oxidative stress; Mitochondria; RNA metabolism; Iron
资金
- ARiSLA (project OligoALS)
- Bruno and Ilse Frick Foundation for ALS research
This review attempts to reconcile the present dual view of the mechanisms operating in Amyotrophic Lateral Sclerosis (ALS). On one side, oxidative stress, mitochondrial damage and protein aggregation are considered as causative of the disease, as strongly supported by evidence obtained in models based on the expression of ALS-typical mutant SOD1. On the other hand, evidence from models expressing ALS-typical mutations in RNA-binding proteins such as FUS and TDP43 indicate that mRNA (dys)metabolism is a major pathway in this disease. A critical analysis of existing literature suggests that there may be more than one point of intersection. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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