Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia

Prog Neurobiol. 2011 Jan;93(1):13-24. doi: 10.1016/j.pneurobio.2010.09.004. Epub 2010 Oct 13.

Abstract

Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem brains, and genetic association studies, have implicated oligodendrocyte and myelin dysfunction in this disease. Recent studies suggest that oligodendrocyte and myelin dysfunction leads to changes in synaptic formation and function, which could lead to cognitive dysfunction, a core symptom of schizophrenia. Furthermore, there is accumulating data linking oligodendrocyte and myelin dysfunction with dopamine and glutamate abnormalities, both of which are found in schizophrenia. These findings implicate oligodendrocyte and myelin dysfunction as a primary change in schizophrenia, not only as secondary consequences of the illness or treatment. Strategies targeting oligodendrocyte and myelin abnormalities could therefore provide therapeutic opportunities for patients suffering from schizophrenia.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Myelin Sheath / pathology
  • Myelin Sheath / physiology*
  • Nerve Net / abnormalities*
  • Nerve Net / physiopathology
  • Oligodendroglia / physiology*
  • Schizophrenia / physiopathology*