Strategies for Oligodendrocyte and Myelin Repair in Traumatic CNS Injury

Anne Huntemer-Silveira, Nandadevi Patil, Megan A. Brickner, Ann M. Parr

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations


A major consequence of traumatic brain and spinal cord injury is the loss of the myelin sheath, a cholesterol-rich layer of insulation that wraps around axons of the nervous system. In the central nervous system (CNS), myelin is produced and maintained by oligodendrocytes. Damage to the CNS may result in oligodendrocyte cell death and subsequent loss of myelin, which can have serious consequences for functional recovery. Demyelination impairs neuronal function by decelerating signal transmission along the axon and has been implicated in many neurodegenerative diseases. After a traumatic injury, mechanisms of endogenous remyelination in the CNS are limited and often fail, for reasons that remain poorly understood. One area of research focuses on enhancing this endogenous response. Existing techniques include the use of small molecules, RNA interference (RNAi), and monoclonal antibodies that target specific signaling components of myelination for recovery. Cell-based replacement strategies geared towards replenishing oligodendrocytes and their progenitors have been utilized by several groups in the last decade as well. In this review article, we discuss the effects of traumatic injury on oligodendrocytes in the CNS, the lack of endogenous remyelination, translational studies in rodent models promoting remyelination, and finally human clinical studies on remyelination in the CNS after injury.

Original languageEnglish (US)
Article number619707
JournalFrontiers in Cellular Neuroscience
StatePublished - Jan 11 2021

Bibliographical note

Publisher Copyright:
© Copyright © 2021 Huntemer-Silveira, Patil, Brickner and Parr.


  • myelin
  • oligodendrocyte
  • remyelination
  • spinal cord injury
  • traumatic injury


Dive into the research topics of 'Strategies for Oligodendrocyte and Myelin Repair in Traumatic CNS Injury'. Together they form a unique fingerprint.

Cite this