Journal of Molecular Neuroscience

, Volume 35, Issue 1, pp 91–100 | Cite as

Lame Ducks or Fierce Creatures? - The Role of Oligodendrocytes in Multiple Sclerosis

Article
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Abstract

In the pathogenesis of multiple sclerosis (MS), oligodendrocytes and its myelin sheaths are thought to be the primary target of destruction. The mechanism leading to oligodendrocyte injury and demyelination is still elusive. Oligodendrocytes are maintaining up to 50 internodes of myelin, which is an extraordinary metabolic demand. This makes them one of the most vulnerable cell types in the central nervous system (CNS), and even small insults can lead to oligodendrocyte impairment, demyelination, and axonal dysfunction. For this reason, oligodendrocytes are viewed as more or less the “lame ducks” of the CNS who can easily become victims. However, recent data demonstrate that this perception possibly needs to be revised. The latest data suggest that oligodendrocytes may also act as “fierce creatures,” influencing the surrounding cells in many ways to preserve its own, as well as their function, allowing sustained functionality of the CNS upon an attack. In this review, the concept of “reactive or activated oligodendrocyte” is introduced, describing alterations in oligodendrocytes which are either protective mechanisms allowing survival in otherwise lethal environment or influence and possibly modulate the ongoing inflammation. Although “harnessed”, oligodendrocytes might actively modulate and shape their environment and be part of the immune privilege of the brain.

Keywords

Oligodendrocyte Oligodendrocyte pathology Normal-appearing white matter Multiple sclerosis Inflammation Innate immunity 
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Notes

Acknowledgements

We thank Prof. Dr. Burkhard Becher (Division of Neuroimmunology, University Hospital Zürich) and Dr. Anna Stalder (Neurobiology, Department of Biomedicine, University Hospital Basel) for the critical reading of the manuscript. This work was supported by the National Multiple Sclerosis Societies of Switzerland, France (ARSEP), United Kingdom, and United States of America.

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© Humana Press 2008

Authors and Affiliations

  1. 1.Neurobiology, Department of BiomedicineUniversity Hospital BaselBaselSwitzerland

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