Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis

作     者：Zhenxiang Gong Li Ba Min Zhang 

作者机构：Department of Neurology and PsychiatryTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China 

出 版 物：《The Journal of Biomedical Research》 (生物医学研究杂志（英文版）)

年 卷 期：2022年第36卷第5期

页      面：336-342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：The current study was supported by the innovative population project of Hubei Province(Grant No.2019CFA030) the clinical research project of Bethune Charitable Foundation,China 

主　　题：oligodendrocytes amyotrophic lateral sclerosis energy metabolism oxidative stress neuroinflammation 

摘      要：Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disorder characterized by irreversible deterioration of upper and lower motor neurons(MNs).Previously,studies on the involvement of glial cells in the pathogenic process of ALS have mainly revolved around astrocytes and *** oligodendrocytes(OLs)have only recently been *** matter demyelination within the motor cortex and proliferation of the oligodendrocyte precursor cells(OPCs)was observed in ALS *** selective ablation of mutant SOD1(the dysfunctional superoxide dismutase)from the oligodendrocyte progenitors after birth significantly delayed disease onset and prolonged the overall survival in ALS mice model(SOD1G37R).In this study,we review the several mechanisms of oligodendrocyte dysfunction involved in the pathological process of myelin damage and MNs death during ***,we examined the insufficient local energy supply from OLs to axons,impaired differentiation from OPCs into OLs mediated by oxidative stress damage,and inflammatory injury to the *** increasing evidence depicted that ALS is not a disease limited to MNs damage,exploring the mechanisms by which oligodendrocyte dysfunction is involved in MNs death would contribute to a more comprehensive understanding of ALS and identifying potential drug targets.