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Oligodendrocyte cell death in pathogenesis of multiple sclerosis: Protection of oligodendrocytes from apoptosis by

Cornelia Cudrici1, Teodora Niculescu, Florin Niculescu

  • 1Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Journal of Rehabilitation Research and Development
|July 19, 2006
PubMed

Insights

Multiple sclerosis involves immune attacks on oligodendrocytes. Complement C5b-9 promotes demyelination in acute MS but may protect these cells in chronic stages.

Area of Science:

  • Neuroimmunology
  • Demyelinating Diseases

Background:

  • Multiple sclerosis (MS) is a chronic central nervous system inflammatory disease.
  • Immune cells and complement system mediate attacks on myelin-forming oligodendrocytes (OLGs).
  • OLG death contributes to demyelination and cell loss in MS plaques.

Purpose of the Study:

  • To investigate the role of complement activation in oligodendrocyte death and demyelination in MS.
  • To elucidate the dual role of complement C5b-9 in acute versus chronic MS pathogenesis.

Main Methods:

  • Studies utilized experimental allergic encephalomyelitis (EAE) models in mice.
  • Experiments involved caspase 11-deficient and C5-deficient mice.
  • Analysis of oligodendrocyte apoptosis, necrosis, and demyelination.

Main Results:

  • Caspase-mediated OLG death is critical for demyelination in EAE.
  • Complement C5b-9 promotes demyelination via the terminal complex.
  • Sublytic C5b-9 protects OLGs from apoptosis, while C5 promotes axon preservation and remyelination.

Conclusions:

  • Activated complement C5b-9 has a dual role in MS pathogenesis.
  • C5b-9 is proinflammatory in acute MS, contributing to demyelination.
  • C5b-9 may offer protection against OLG death in chronic MS through promoting remyelination.

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