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Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population.

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Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population. / Grabe, Hans Jörgen; Schwahn, Christian; Appel, Katja; Mahler, Jessie; Schulz, Andrea; Spitzer, Carsten; Fenske, Kristin; Barnow, Sven; Lucht, Michael; Freyberger, Harald Jürgen; John, Ulrich; Teumer, Alexander; Wallaschofski, Henri; Nauck, Matthias; Völzke, Henry.

In: AM J MED GENET B, Vol. 153, No. 8, 8, 2010, p. 1483-1493.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Grabe, HJ, Schwahn, C, Appel, K, Mahler, J, Schulz, A, Spitzer, C, Fenske, K, Barnow, S, Lucht, M, Freyberger, HJ, John, U, Teumer, A, Wallaschofski, H, Nauck, M & Völzke, H 2010, 'Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population.', AM J MED GENET B, vol. 153, no. 8, 8, pp. 1483-1493. <http://www.ncbi.nlm.nih.gov/pubmed/20957648?dopt=Citation>

APA

Grabe, H. J., Schwahn, C., Appel, K., Mahler, J., Schulz, A., Spitzer, C., Fenske, K., Barnow, S., Lucht, M., Freyberger, H. J., John, U., Teumer, A., Wallaschofski, H., Nauck, M., & Völzke, H. (2010). Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population. AM J MED GENET B, 153(8), 1483-1493. [8]. http://www.ncbi.nlm.nih.gov/pubmed/20957648?dopt=Citation

Vancouver

Grabe HJ, Schwahn C, Appel K, Mahler J, Schulz A, Spitzer C et al. Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population. AM J MED GENET B. 2010;153(8):1483-1493. 8.

Bibtex

@article{2b360876c6e84cbc824c24cb2e5d2c0a,
title = "Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population.",
abstract = "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. {\textcopyright} 2010 Wiley-Liss, Inc.",
author = "Grabe, {Hans J{\"o}rgen} and Christian Schwahn and Katja Appel and Jessie Mahler and Andrea Schulz and Carsten Spitzer and Kristin Fenske and Sven Barnow and Michael Lucht and Freyberger, {Harald J{\"u}rgen} and Ulrich John and Alexander Teumer and Henri Wallaschofski and Matthias Nauck and Henry V{\"o}lzke",
year = "2010",
language = "Deutsch",
volume = "153",
pages = "1483--1493",
journal = "AM J MED GENET B",
issn = "1552-4841",
publisher = "Wiley-Liss Inc.",
number = "8",

}

RIS

TY - JOUR

T1 - Childhood maltreatment, the corticotropin-releasing hormone receptor gene and adult depression in the general population.

AU - Grabe, Hans Jörgen

AU - Schwahn, Christian

AU - Appel, Katja

AU - Mahler, Jessie

AU - Schulz, Andrea

AU - Spitzer, Carsten

AU - Fenske, Kristin

AU - Barnow, Sven

AU - Lucht, Michael

AU - Freyberger, Harald Jürgen

AU - John, Ulrich

AU - Teumer, Alexander

AU - Wallaschofski, Henri

AU - Nauck, Matthias

AU - Völzke, Henry

PY - 2010

Y1 - 2010

N2 - 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. © 2010 Wiley-Liss, Inc.

AB - 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. © 2010 Wiley-Liss, Inc.

M3 - SCORING: Zeitschriftenaufsatz

VL - 153

SP - 1483

EP - 1493

JO - AM J MED GENET B

JF - AM J MED GENET B

SN - 1552-4841

IS - 8

M1 - 8

ER -