Journal
AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
Volume 153B, Issue 8, Pages 1483-1493Publisher
WILEY
DOI: 10.1002/ajmg.b.31131
Keywords
major depression; hypothalamic-pituitary-adrenal (HPA) axis; childhood neglect; general population; epidemiology; CRHR1 gene; gene-environment interaction
Categories
Funding
- German Research Foundation
- Federal Ministry of Education and Research Germany
- Janssen-Cilag
- Eli Lilly
- Novartis
- AstraZeneca
- SALUS-Institute for Trend-Research and Therapy Evaluation in Mental Health
- Boehringer Ingelheim
- Stiftung zur Aufarbeitung der SED-Diktatur
- Federal Ministry of Health Germany
- Federal Ministry of Education and Research [01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012]
- Social Ministry of the Federal State of Mecklenburg-West Pomerania
- Family Ministry of the Federal Republic of Germany
- German Cancer Aid
- European Union
- Social Ministry of the Federal State of Mecklenburg-West Pomerania of Germany
- Pfizer
- Novo Nordisc
- Sanofi-Aventis
- BioRad Laboratories GmbH
- Siemens AG
- Zeitschrift fur Laboratoriumsmedizin
- Bruker Daltronics
- Abbott
- Jurilab Kuopio
- Roche Diagnostics
- Dade Behring
- DPC Biermann
- Becton Dickinson
- Biotronik
- Humboldt Foundation
- Ministry of Cultural Affairs
- Siemens Healthcare, Erlangen, Germany
- Federal State of Mecklenburg-West Pomerania
- German Research Foundation (DFG) [GR 1912/5-1]
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Dysregulations of the hypothalamic-pituitary-adrenal (HPA) axis have been implicated in the pathogenesis of depressive disorders and the corticotropin-releasing hormone (CRH) was found to modulate emotional memory consolidation. Recently, two studies have reported an interaction between childhood abuse and the TAT-haplotype of the CRH-Receptor Gene (CRHR1) connecting childhood adversities and genetic susceptibility to adult depression. We tested the hypothesis of an interaction of childhood maltreatment with single nucleotide polymorphisms (SNPs) and haplotypes of the CRHR1 gene not previously investigated. Caucasian subjects (n = 1,638) from the German general population (Study of Health in Pomerania, SHIP) were analyzed. As in the previous studies, childhood abuse and neglect were assessed with the Childhood Trauma Questionnaire (CTQ) and depression with the Beck Depression Inventory (BDI-2). The CRHR1-SNPs were genotyped on the Affymetrix Genome-Wide Human SNP Array 6.0 platform. We identified an interaction between the TAT-haplotype and childhood physical neglect. The interaction with physical neglect showed significant (P < 0.05) results in 23 of the 28 SNPs, with rs17689882 (P = 0.0013) reaching gene-wide'' significance. Although we did not replicate the specific interaction of abuse and the TAT-haplotype of the CRHR1 gene we confirmed the relevance of an interplay between variants within the CRHR1 gene and childhood adversities in the modulation of depression in adults. The largest effect was found for rs17689882, a SNP previously not analyzed. Relevant sample differences between this and prior studies like lower BDI-2 scores, less childhood maltreatment and higher psychosocial functioning may account for the differences in gene-environment interaction findings. (C) 2010 Wiley-Liss, Inc.
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