Abstract

We carried out whole-exome ultra-high throughput sequencing in brain samples of suicide victims who had suffered from major depressive disorder and control subjects who had died from other causes. This study aimed to reveal the selective accumulation of rare variants in the coding and the UTR sequences within the genes of suicide victims. We also analysed the potential effect of STR and CNV variations, as well as the infection of the brain with neurovirulent viruses in this behavioural disorder. As a result, we have identified several candidate genes, among others three calcium channel genes that may potentially contribute to completed suicide. We also explored the potential implication of the TGF-β signalling pathway in the pathogenesis of suicidal behaviour. To our best knowledge, this is the first study that uses whole-exome sequencing for the investigation of suicide.

Details

Title
High-Coverage Whole-Exome Sequencing Identifies Candidate Genes for Suicide in Victims with Major Depressive Disorder
Author
Tombácz, Dóra 1 ; Maróti, Zoltán 2 ; Kalmár, Tibor 2   VIAFID ORCID Logo  ; Csabai, Zsolt 3 ; Balázs, Zsolt 3 ; Takahashi, Shinichi 4 ; Palkovits, Miklós 5 ; Snyder, Michael 4 ; Boldogkői, Zsolt 3 

 Department of Medical Biology, Faculty of Medicine, University of Szeged, Szeged, Hungary; Department of Genetics, School of Medicine, Stanford University, Stanford, CA, USA 
 Department of Paediatrics, Faculty of Medicine, University of Szeged, Szeged, Hungary 
 Department of Medical Biology, Faculty of Medicine, University of Szeged, Szeged, Hungary 
 Department of Genetics, School of Medicine, Stanford University, Stanford, CA, USA 
 Neuromorphological and Neuroendocrine Research Laboratory, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary 
Pages
1-11
Publication year
2017
Publication date
Aug 2017
Publisher
Nature Publishing Group
e-ISSN
20452322
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1957127774
Copyright
© 2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.