, Volume 10, Issue 4, pp 757–770

Epigenetics of Neural Repair Following Spinal Cord Injury


DOI: 10.1007/s13311-013-0228-z

Cite this article as:
York, E.M., Petit, A. & Roskams, A.J. Neurotherapeutics (2013) 10: 757. doi:10.1007/s13311-013-0228-z


Spinal cord injury results from an insult inflicted on the spinal cord that usually encompasses its 4 major functions (motor, sensory, autonomic, and reflex). The type of deficits resulting from spinal cord injury arise from primary insult, but their long-term severity is due to a multitude of pathophysiological processes during the secondary phase of injury. The failure of the mammalian spinal cord to regenerate and repair is often attributed to the very feature that makes the central nervous system special—it becomes so highly specialized to perform higher functions that it cannot effectively reactivate developmental programs to re-build novel circuitry to restore function after injury. Added to this is an extensive gliotic and immune response that is essential for clearance of cellular debris, but also lays down many obstacles that are detrimental to regeneration. Here, we discuss how the mature chromatin state of different central nervous system cells (neural, glial, and immune) may contribute to secondary pathophysiology, and how restoring silenced developmental gene expression by altering histone acetylation could stall secondary damage and contribute to novel approaches to stimulate endogenous repair.


InflammationRegenerationNeuroprotectionMyelin repairNeuroglial progenitors

Supplementary material

13311_2013_228_MOESM1_ESM.pdf (1.2 mb)
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Copyright information

© The American Society for Experimental NeuroTherapeutics, Inc. 2013

Authors and Affiliations

  • Elisa M. York
    • 1
  • Audrey Petit
    • 1
  • A. Jane Roskams
    • 1
  1. 1.Department of Zoology (Life Sciences Institute), Brain Research Institute and International Collaboration on Repair Discoveries (iCORD)University of British ColumbiaVancouverCanada