Molecular mechanisms of oligodendrocyte injury in multiple sclerosis and experimental autoimmune encephalomyelitis

Jilpa Patel, Roumen Balabanov*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

35 Scopus citations


New evidence has emerged over the last decade indicating that oligodendrocyte injury in multiple sclerosis (MS) is not a single unified phenomenon but rather a spectrum of processes ranging from massive immune destruction to a subtle cell death in the absence of significant inflammation. Experimentally, protection of oligodendrocytes against inflammatory injury results in protection against experimental autoimmune encephalitis, the animal model of multiple sclerosis. In this review, we will discuss the molecular mechanisms regulating oligodendrocyte injury and inflammatory demyelination. We draw attention to the injurious role of IFN-γ signaling in oligodendrocytes and the pro-inflammatory effect of their death. In conclusion, studying the molecular mechanisms of oligodendrocyte injury is likely to provide new perspective on the pathogenesis of MS and a rationale for cell protective therapies.

Original languageEnglish (US)
Pages (from-to)10647-10659
Number of pages13
JournalInternational journal of molecular sciences
Issue number8
StatePublished - Aug 2012


  • Caspase 1
  • Cell signaling
  • Interferon regulatory factor 1
  • Multiple sclerosis
  • Oligodendrocytes
  • Pathology

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry


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