Abstract
Schizophrenia (SZ) is a chronic and severe mental illness for which currently there is no cure. At present, the exact molecular mechanism involved in the underlying pathogenesis of SZ is unknown. The disease is thought to be caused by a combination of genetic, biological, psychological, and environmental factors. Recent studies have shown that epigenetic regulation is involved in SZ pathology. Specifically, DNA methylation, one of the earliest found epigenetic modifications, has been extensively linked to modulation of neuronal function, leading to psychiatric disorders such as SZ. However, increasing evidence indicates that glial cells, especially dysfunctional oligodendrocytes undergo DNA methylation changes that contribute to the pathogenesis of SZ. This review primarily focuses on DNA methylation involved in glial dysfunctions in SZ. Clarifying this mechanism may lead to the development of new therapeutic interventional strategies for the treatment of SZ and other illnesses by correcting abnormal methylation in glial cells.
Highlights
Schizophrenia (SZ) is a chronic and severe mental illness that affects approximately 1% of the population (Roussos and Haroutunian, 2014)
We primarily focus on the role of DNA methylation in glial cells’ generation and aberrant methylation involved in glial dysfunction leading to SZ and other related illnesses
Notch signaling, the hypoxiainducible factor 1a (HIF1α), Old astrocyte induced substance (OASIS), the murine homologs of chicken ovalbumin upstream promoter transcription factors I and II (COUPTFI/II) are typical target molecules that contribute to the demethylation of the Gfap promoter (Naka et al, 2008; Mutoh et al, 2012; Saito et al, 2012)
Summary
Schizophrenia (SZ) is a chronic and severe mental illness that affects approximately 1% of the population (Roussos and Haroutunian, 2014). Antipsychotic drugs have been shown to be able to alter the pathological changes associated with DNA methylation or demethylation and are thereby thought to be beneficial in the treatment of SZ (reviewed in Guidotti and Grayson, 2014). In this comprehensive review, we primarily focus on the role of DNA methylation in glial cells’ generation and aberrant methylation involved in glial dysfunction leading to SZ and other related illnesses
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