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Association analyses of depression and genes in the hypothalamus–pituitary–adrenal axis

Published online by Cambridge University Press:  06 June 2016

Henrietta Nørmølle Buttenschøn*
Affiliation:
Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov, Denmark The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Aarhus, Denmark
Jesper Krogh
Affiliation:
Mental Health Center Copenhagen, Mental Health Services in Capital Region, University of Copenhagen, Copenhagen, Denmark
Marit Nyholm Nielsen
Affiliation:
Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov, Denmark The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Aarhus, Denmark
Linda Kaerlev
Affiliation:
Research Unit of Clinical Epidemiology, Institute of Clinical Research, University of Southern Denmark, Odense, Denmark Center for Clinical Epidemiology, Odense University Hospital, Odense, Denmark
Merete Nordentoft
Affiliation:
The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Aarhus, Denmark Mental Health Center Copenhagen, Mental Health Services in Capital Region, University of Copenhagen, Copenhagen, Denmark
Ole Mors
Affiliation:
The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Aarhus, Denmark Psychosis Research Unit, Aarhus University Hospital, Risskov, Denmark
*
Henriette Nørmølle Buttenschøn, Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Skovagervej 2, 8240 Risskov, Denmark. Tel: +45 78471163; Fax: +45 78471108; E-mail: [email protected]

Abstract

Objective

Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis has been reported in depression. The aim was to investigate the potential association between depression and seven genes regulating or interfering with the HPA axis, including the gene encoding angiotensin converting enzyme (ACE).

Methods

In total, 78 single nucleotide polymorphisms (SNPs) and one insertion/deletion polymorphism were genotyped. The study included 408 individuals with depression and 289 controls. In a subset of cases, the interaction between genetic variants and stressful life events (SLEs) was investigated.

Results

After quality control, 68 genetic variants were left for analyses. Four of nine variants within ACE were nominally associated with depression and a gene-wise association was likewise observed. However, none of the SNPs located within AVP, CRH, CRHR1, CRHR2, FKBP5 or NC3C1 were associated with depression. One nominally significant interaction, most likely due to chance, was identified.

Conclusion

The results indicate that ACE could be a potential candidate gene for depression.

Type
Short Communication
Copyright
© Scandinavian College of Neuropsychopharmacology 2016 

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