Mending the broken in amyotrophic lateral sclerosis: DNA damage and repair in motor neuron degeneration

作     者：Byung Woo Kim Lee J.Martin Byung Woo Kim;Lee J.Martin

作者机构：Department of PathologyDivision of Neuropathologythe Pathobiology Graduate Training ProgramJohns Hopkins University School of MedicineBaltimoreMDUSA Department of NeuroscienceJohns Hopkins University School of MedicineBaltimoreMDUSA 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2021年第16卷第1期

页      面：104-105页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by grants from the U.S.Public Health Service NIH-NINDS(NS034100,NS065895,NS052098,NS079348) NIH-NIA (AG016282) 

主　　题：al. damage degeneration 

摘      要：Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disease that causes paralysis and respiratory failure(Petrov et al.,2017).The driving mechanisms are unknown,and there are no effective treatments(Petrov et al.,2017).Aging and a few gene mutations,a common one being missense mutations in superoxide dismutase-1(SOD1),are risk factors for ALS(Figure 1).The recent Food and Drug Administration approval of edaravone for the treatment of ALS putatively supports a role for oxidative and nitrative stresses in the disease processes(Figure 1A).DNA damage,abnormalities in DNA repair,and other nuclear abnormalities are implicated also in the pathogenesis of human ALS(Bradley and Krasin,1982;Kim et al.,2020).