Oligodendrocyte Progenitors in Schizophrenia: The Role in Pathogenesis and Potential Treatment Target

Abstract

Background:  schizophrenia is considered as a dysconnectivity disorder supported by neuroimaging studies have revealed altered myelination of white and grey matter. Altered myelination suggests oligodendrocyte (OL) family pathology. Oligodendrocyte progenitors (OP) are of special interest since they myelinate axons in mature brain at the last stage of the differentiation. The aim of review  —  to summarize modern research data concerning altered cell cycle of OL family in schizophrenia and their plausible reason. Material and methods: using the keywords “schizophrenia, OL, OP”, “OP and schizophrenia risk genes”, “OP and neuroinflamation”, “OP and antipsychotic drugs”, “OP, dopamine, serotonin” 164 studies concerning the influence of listed above factors on OP differentiation were selected the MedLine/PubMed, Google Scholar, eLibrary databases for analysis.  Conclusion: postmortem studies demonstrated essential deficit of OL family cells as well as altered correlation pattern between the number of these cells suggested altered OP differentiation. Some of OL and myelin-related gene variants caused higher schizophrenia risk play a critical role in OP differentiation. While neuroinflammation is important component of schizophrenia brain pathology proinflammatory cytokines and activated microglia exert substantial influence on OP proliferation and differentiation. Atypical antipsychotics are able to correct OP maturation and have anti-inflammatory effects. OL and OP as well as microglia and peripheral immune cells express dopamine and serotonin receptors, main  therapeutic targets of these drugs. OP pathology as important component of schizophrenia  pathogenesis, tightly linked with another abnormalities, and considers as promising target for future therapeutic strategy.