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Editorial: Neuroepigenetics of Neuropsychiatric Disease-Hope, Success and Obstacles for Translational Findings and Applications
Linde and Zimmer-Bensch discuss the role of DNA methylation and its writers, DNA methyltransferases DNMT1 and DNMT3A, in regulating essential genes for GABAergic neuronal functions, as well as genes of the endocytosis process critical for synaptic neurotransmission. Besides perturbations in neurons,...
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Published in: | Frontiers in neuroscience 2022-04, Vol.16, p.886695-886695 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Linde and Zimmer-Bensch discuss the role of DNA methylation and its writers, DNA methyltransferases DNMT1 and DNMT3A, in regulating essential genes for GABAergic neuronal functions, as well as genes of the endocytosis process critical for synaptic neurotransmission. Besides perturbations in neurons, glia pathology also participates in psychiatric disorders (Cotter et al., 2002). Since DNA methylation is critically implicated in many neuropsychiatric diseases, it presents a potential target for treatment (Sales and Joca, 2016; Shirvani-Farsani et al., 2021). Among all these studies, only the correlation between methylation at the BDNF gene locus and antidepressant effects in MDD was reproduced by multiple groups (Januar et al., 2015; Zhou et al.). Since the antidepressant effect of BDNF is well-established in animal studies (Lee and Kim, 2010), this provides evidence for using current animal models (stress-induced depressive-like behaviors in mice and rats) as valid tools for studying mental disorders. MDD is becoming one of the most severe health problems globally (Otte et al., 2016). Besides chronic stress that is well-accepted as top one risk factor for MDD (Breslau and Davis, 1986), other environmental factors, including dietary influences, contribute to the neuropathogenesis of depression (Firth et al., 2020). |
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ISSN: | 1662-4548 1662-453X 1662-453X |
DOI: | 10.3389/fnins.2022.886695 |