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.

Original languageEnglish
Pages (from-to)13-24
Number of pages12
JournalProgress in Neurobiology
Volume93
Issue number1
DOIs
StatePublished - Jan 2011

Keywords

  • Brain imaging
  • Dopamine
  • Gene expression
  • Genetic association
  • Glutamate
  • Myelin
  • Oligodendrocyte
  • Synaptic plasticity

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