Brief Research Communication
Dopamine beta-hydroxylase (DBH) activity and -1021C/T polymorphism of DBH gene in combat-related post-traumatic stress disorder†
Article first published online: 12 SEP 2007
Copyright © 2007 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume 144B, Issue 8, pages 1087–1089, 5 December 2007
How to Cite
Mustapić, M., Pivac, N., Kozarić-Kovačić, D., Deželjin, M., Cubells, J. F. and Mück-Šeler, D. (2007), Dopamine beta-hydroxylase (DBH) activity and -1021C/T polymorphism of DBH gene in combat-related post-traumatic stress disorder. Am. J. Med. Genet., 144B: 1087–1089. doi: 10.1002/ajmg.b.30526
Please cite this article as follows: Mustapić M, Pivac N, Kozarić-Kovačić D, Deželjin M, Cubells JF, Mück-Šeler D. 2007. Dopamine Beta-Hydroxylase (DBH) Activity and −1021C/T Polymorphism of DBH Gene in Combat-Related Post-Traumatic Stress Disorder. Am J Med Genet Part B 144B:1087–1089.
- Issue published online: 13 NOV 2007
- Article first published online: 12 SEP 2007
- Manuscript Accepted: 15 FEB 2007
- Manuscript Received: 6 NOV 2006
- DBH polymorphism;
- posttraumatic stress disorder;
- war veterans
The roles of dopamine (DA) and norepinephrine (NE) in posttraumatic stress disorder (PTSD) are unclear. The aim of the study was to determine plasma dopamine beta-hydroxylase (DBH) activity and DBH-1021C/T gene polymorphism in combat veterans with (N = 133) or without (N = 34) chronic PTSD. Similar frequencies in genotype or allele distribution were found between veterans with or without PTSD. War veterans with PTSD had lower DBH activity, associated with the DBH-1021C/T variant in DBH genes, than veterans without PTSD. A significantly lower plasma DBH activity was found in combat veterans with PTSD carrying the CC genotype as compared to veterans without PTSD carrying the corresponding genotype. Since both groups were exposed to the same trauma, it is possible that a pre-existing trait difference in regulation of NE function contributed to a differential vulnerability to develop PTSD, or that the regulation of DBH expression was different in response to trauma. The results suggest that that genotype-controlled measurement of plasma DBH activity might be used as a potential biological marker of the response to trauma, and that further studies of DBH and other loci related to DA and NA in PTSD are warranted. © 2007 Wiley-Liss, Inc.