"Locomotor Recovery Following Moderate or Severe Contusive Spinal Cord Injury does not Require Oligodendrocyte Remyelination" - Wolfram Tetzlaff, MD, PhD | John and Penny Ryan BC Leadership Chair in Spinal Cord Research; Professor, University of BC
Spinal cord injury (SCI) can lead to severe and permanent motor, sensory and autonomic dysfunction due to the adult mammalian spinal cord’s inability to regenerate lost neurons and their connections. Most SCIs in humans do not result in the complete transection of the spinal cord but instead axons are spared at the lesion epicenter and a period of limited functional improvement commences soon after SCI despite axon regeneration failure. Enhancing the functional connectivity of the spared circuitry may be a viable means of promoting functional improvements following SCI. However, oligodendrocyte death in the weeks after SCI presumably results in the demyelination of spared axons, which could diminish the functionality of spared circuits. Demyelination impairs the amplitude and speed of electrical conductance and oligodendrocyte loss may leave axons vulnerable to degeneration. For these reasons, strategies to enhance oligodendrocyte remyelination of spared axons have been hypothesized to promote functional improvements following SCI. However, the extent of remyelination and its role of myelin regeneration in locomotor recovery has never been tested directly. Our data indicates that while spontaneous remyelination is extensive following SCI, it is not associated with improvements in hindlimb motor function during spontaneous recovery in our contusion models. This questions the interpretation/validity of rodent models used in support of clinical trials of transplantation of oligodendrocytes precursor cells.
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