Henrietta Nørmølle Buttenschøn1, Jesper Krogh2, Marit Nyholm Nielsen1, Linda Kaerlev3, Merete Nordentoft4, Ole Mors4. 1. 1Translational Neuropsychiatry Unit,Department of Clinical Medicine,Aarhus University,Risskov,Denmark. 2. 3Mental Health Center Copenhagen,Mental Health Services in Capital Region,University of Copenhagen,Copenhagen,Denmark. 3. 4Research Unit of Clinical Epidemiology,Institute of Clinical Research,University of Southern Denmark,Odense,Denmark. 4. 2The Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH),Aarhus,Denmark.
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.
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.
Authors: Lotte Gerritsen; Yuri Milaneschi; Christiaan H Vinkers; Albert M van Hemert; Laura van Velzen; Lianne Schmaal; Brenda Wjh Penninx Journal: Neuropsychopharmacology Date: 2017-06-07 Impact factor: 7.853