Dissecting the molecular mechanisms of gene x environment interactions: implications for diagnosis and treatment of stress-related psychiatric disorders

• Type of Material: Article
• Authors: Elisabeth B. Binder, Emory University
• Language: English
• Date: 2017-01-01
• Publisher: Taylor & Francis Open: Creative Commons Attribution
• Publication Version: Final Published Version
• Copyright Statement: © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1080/20008198.2017.1412745
• Title of Journal or Parent Work: European Journal of Psychotraumatology
• ISSN: 2000-8066
• Volume: 8
• Issue: sup5
• Start Page: 1412745
• End Page: 1412745
• Grant/Funding Information: The author receives funding from the National Institute of Mental Health (NIMH), the German Federal Ministry of Health and Education (BMBF), the Jacobs-Foundation as well as a research grant from Böhringer Ingelheim to study FKBP5 as a potential target for antidepressant treatment.
• Keywords: DNA DEMETHYLATION; METHYLATION; Psychology; Psychiatry; FKBP5 GENOTYPE; Psychology, Clinical; ASSOCIATIONS; Science & Technology; CHILDHOOD ADVERSITY; Social Sciences; early adversity; DEPRESSIVE EPISODES; Gene x environment interaction; NATIONAL COMORBIDITY SURVEY; Life Sciences & Biomedicine; CONNECTIVITY; DNA methylation; POLYMORPHISMS; GLUCOCORTICOID-RECEPTOR; epigenetics
• Research Categories: Psychology, Behavioral

Abstract

© 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. Epidemiological studies indicate a combined contribution of genetic and environmental factors, mainly exposure to adverse life events, in the risk for psychiatric disease. Understanding how adverse life events interact with genetic predisposition on the molecular level to shape risk and resilience to psychiatric disorders may yield important insight into disease mechanism. Using the example of the molecular mechanisms of interaction of functional genetic variants within the stress-regulating gene FKBP5 and early adversity, it is delineated how this interaction could contribute to transdiagnostic disease risk via a combined genetic and epigenetic disinhibition of FKBP5 transcription. This knowledge may now allow to develop biomarkers for a transdiagnostic subset of psychiatric patients and to personalize treatment.