The association of childhood maltreatment with depression and anxiety is not moderated by the oxytocin receptor gene

The association of childhood maltreatment with depression and anxiety is not moderated by the... Eur Arch Psychiatry Clin Neurosci (2017) 267:517–526 DOI 10.1007/s00406-017-0784-z ORIGINAL PAPER The association of childhood maltreatment with depression and anxiety is not moderated by the oxytocin receptor gene 1 1 2 Marieke S. Tollenaar  · Marc L. Molendijk  · Brenda W. J. H. Penninx  · 2 1 Yuri Milaneschi  · Niki Antypa   Received: 23 August 2016 / Accepted: 13 March 2017 / Published online: 28 March 2017 © The Author(s) 2017. This article is an open access publication Abstract the OXTR SNPs did not moderate these associations nor Background The oxytocin receptor (OXTR) gene may had main effects on outcomes. be involved in resilience or vulnerability towards stress, Conclusions The three OXTR gene SNPs did not interact and hence in the development of stress-related disorders. with childhood maltreatment in predicting lifetime depres- There are indications that OXTR single nucleotide poly- sion and anxiety diagnoses or sensitivity. This stresses the morphisms (SNPs) interact with early life stressors in pre- importance of replication studies with regard to OXTR dicting levels of depression and anxiety. To replicate and gene variants in general populations as well as in clearly extend these findings, we examined whether three litera- established clinical samples. ture-based OXTR SNPs (rs2254298, rs53576, rs2268498) interact with childhood maltreatment in the development of Keywords OXTR · Oxytocin · Single nucleotide http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Archives of Psychiatry and Clinical Neuroscience Springer Journals

The association of childhood maltreatment with depression and anxiety is not moderated by the oxytocin receptor gene

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by The Author(s)
Subject
Medicine & Public Health; Psychiatry; Neurosciences; Neurology
ISSN
0940-1334
eISSN
1433-8491
D.O.I.
10.1007/s00406-017-0784-z
Publisher site
See Article on Publisher Site

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