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Schizophrenia is a severe psychiatric disorder with complex clinical manifestations and its aetiological factors remain unclear. During the past decade, the oligodendrocyte-related myelin dysfunction was proposed as a hypothesis for schizophrenia, supported initially by a series of neuroimaging studies and genetic evidence. Recently, the effects of antipsychotics on myelination and oligodendroglial lineage development and their underlying molecular mechanisms were evaluated. Data from those studies suggest that the antipsychotics-resulting improvement in myelin/oligodendrocyte-related dysfunction may contribute, at least in part, to their therapeutic effect on schizophrenia. Importantly, these findings may provide the basis for a new insight into the therapeutic strategy by targeting the oligodendroglia lineage cells against schizophrenia.

Improving myelin/oligodendrocyte-related dysfunction: a new mechanism of antipsychotics in the treatment of schizophrenia?