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Myelin impairs CNS remyelination by inhibiting oligodendrocyte precursor cell differentiation

Mark R Kotter1, Wen-Wu Li, Chao Zhao

  • 1Cambridge Centre for Brain Repair, Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|January 10, 2006
PubMed

Insights

Myelin debris in demyelinated lesions inhibits central nervous system (CNS) repair. This study shows myelin prevents oligodendrocyte precursor cell differentiation, impairing remyelination in multiple sclerosis models.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Demyelination in the adult central nervous system (CNS) can be repaired.
  • Multiple sclerosis (MS) involves inhibited oligodendrocyte differentiation in lesions.
  • Myelin debris is present in demyelinated lesions and inhibits oligodendrocyte precursor cell differentiation in vitro.

Purpose of the Study:

  • To investigate the effect of myelin debris on remyelination efficiency in a demyelinated lesion model.
  • To determine if myelin debris inhibits oligodendrocyte precursor cell differentiation or recruitment in vivo.

Main Methods:

  • Focal demyelinating lesions were induced in the adult rat brainstem.
  • Naturally occurring myelin debris was increased by adding purified myelin.
  • Myelin basic protein mRNA expression was quantified using laser capture microdissection.
  • Histological analysis was performed to assess remyelination and cell differentiation.

Main Results:

  • Increased myelin debris significantly impaired remyelination.
  • Remyelination failure was due to an arrest in oligodendrocyte precursor cell differentiation, not impaired recruitment.
  • Myelin acts as an inhibitor of CNS remyelination.

Conclusions:

  • Myelin debris is a key factor inhibiting remyelination in the CNS.
  • Targeting myelin debris may enhance repair in demyelinating diseases like MS.
  • These findings identify myelin as a barrier to CNS repair, similar to its known effect on axon regeneration.

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