Abstract
Schizophrenia is a complex neuropsychiatric disorder affected by both genetic and epigenetic factors. Except for neuronal dysfunction, oligodendroglial abnormalities also contribute to the disease pathogenesis, characterized by a robust dysregulation of oligodendrocyte and myelin related genes. Accumulating evidence shows that histone modifications play important roles in transcriptional regulation of the genes crucial for oligodendrocyte differentiation and myelination. Specifically, the histone acetylation and methylation were two well-recognized histone modification abnormalities in the schizophrenic brains. In this mini-review, we will describe the dynamic changes of histone acetylation and methylation in schizophrenia, which may coordinate and induce deleterious epigenetic memory in oligodendroglial cells, and further lead to oligodendrocyte and myelin deficits. Precise modulation of histone modification status in oligodendroglial cells needs to secure the balance of epigenetic marks, which may revise the therapeutic strategy for the white matter etiology of neuropsychiatric disorders.
Highlights
Schizophrenia is a severe and heterogeneous psychiatric disorder that affects about one percent of the world’s population (Jauhar et al, 2022)
Together with Liu et al, we reported that social deprivation, a well-defined environmental risk factor of schizophrenia, could affect H3K9 tri-methylation status in OLs, which could be responsible for OLs dysfunction and myelin deficits in the prefrontal cortex (Liu et al, 2012; Chen et al, 2019)
Since histone acetylation and methylation enzymes activity are robustly dysregulated in schizophrenia (Peter and Akbarian, 2011; Qiu et al, 2017), they may disturb the epigenetic memory in OLs during the pathogenesis, and further lead to the heterochronic expression of transcriptional inhibitors in mature OLs
Summary
Schizophrenia is a severe and heterogeneous psychiatric disorder that affects about one percent of the world’s population (Jauhar et al, 2022). Recent study found that blocking HDAC activity impairs the OPC early differentiation, but does not affect myelin gene expression after initiating myelination (Shen et al, 2005).
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