• ISSN 1674-8301
  • CN 32-1810/R
Volume 36 Issue 5
Sep.  2022
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Zhenxiang Gong, Li Ba, Min Zhang. Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis[J]. The Journal of Biomedical Research, 2022, 36(5): 336-342. doi: 10.7555/JBR.36.20220009
Citation: Zhenxiang Gong, Li Ba, Min Zhang. Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis[J]. The Journal of Biomedical Research, 2022, 36(5): 336-342. doi: 10.7555/JBR.36.20220009

Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis

doi: 10.7555/JBR.36.20220009
Funds:  The current study was supported by the innovative population project of Hubei Province (Grant No. 2019CFA030) and the clinical research project of Bethune Charitable Foundation, China.
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  • Corresponding author: Min Zhang, Department of Neurology and Psychiatry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Road, Qiaokou District, Wuhan, Hubei 430030, China. Tel: +86-27-83663895, E-mail: zhang_min_3464@126.com
  • Received: 2022-01-10
  • Revised: 2022-06-13
  • Accepted: 2022-07-04
  • Published: 2022-08-28
  • Issue Date: 2022-09-28
  • 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 microglia. And oligodendrocytes (OLs) have only recently been highlighted. Grey matter demyelination within the motor cortex and proliferation of the oligodendrocyte precursor cells (OPCs) was observed in ALS patients. The 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 ALS. Particularly, 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 OLs. Since 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.


  • CLC number: R744.8, Document code: A
    The authors reported no conflict of interests.
    These authors contributed to this work equally.
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