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Epigenetics and depression

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Penner-Goeke,  Signe
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Binder,  Elisabeth B.
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Penner-Goeke, S., & Binder, E. B. (2019). Epigenetics and depression. Dialogues in Clinical Neuroscience, 21(4), 397-405. doi:10.31887/DCNS.2019.21.4/ebinder.


Cite as: https://hdl.handle.net/21.11116/0000-0005-F7D6-3
Abstract
The risk for major depression is both genetically and environmentally determined. It has been proposed that epigenetic mechanisms could mediate the lasting increases in depression risk following exposure to adverse life events and provide a mechanistic framework within which genetic and environmental factors can be integrated. Epigenetics refers to processes affecting gene expression and translation that do not involve changes in the DNA sequence and include DNA methylation (DNAm) and micro NAs (miRNAs) as well as histone modifications. ere we review evidence for a role of epigenetics in the pathogenesis of depression from studies investigating DNAm, miRNAs, and histone modifications using different tissues and various experimental designs. From these studies, a model emerges where underlying genetic and environmental risk factors, and interactions between the two, could drive aberrant epigenetic mechanisms targeting stress response pathways, neuronal plasticity, and other behaviorally relevant pathways that have been implicated in major depression. (C) 2019, AICH - Servier Group.