As schizophrenia is a complex mental disorder and the outcome of gene-gene-environmental interactions, there are different possible pathophysiological mechanisms in different schizophrenia subtypes corresponding to various risk factors. This study was aimed at examining the impact of one of the most likely interactions, that is, ‘dopamine and stress’, in schizophrenia pathogenesis.
Here, we investigated the interaction between ‘war-related psychological trauma’ without brain trauma and catechol-O-methyltransferase gene. Using real-time PCR analysis we measured catechol-O-methyltransferase gene expression level in the blood cells of 66 male subjects in four groups, namely veteran schizophrenia patients as ‘stress-exposed schizophrenia’ (S-schizophrenia), their healthy brothers as ‘their genetically closest relatives’ (S-siblings), schizophrenia patients without any history of significant stress as ‘non-stress-exposed schizophrenia’ (NoS-schizophrenia), and the control group. The results were analyzed by Relative Expression Software Tool 2009 software.
The catechol-O-methyltransferase gene expression was not significantly different between the S-schizophrenia and NoS-schizophrenia groups. However, compared to the control group, the catechol-O-methyltransferase expression was significantly decreased in three groups of S-schizophrenia, their healthy siblings, and NoS-schizophrenia patients.
This data supports that reduced blood catechol-O-methyltransferase expression, which may be associated with higher dopamine level, is involved both in stress-induced and non-stress–induced schizophrenia.
aDepartment of Neuroscience and addiction studies, School of Advanced Technologies in Medicine
bResearch Center for Cognitive and Behavioral Sciences
cMedical Genetics Department
iDepartment of Pharmacology, School of Medicine
eDepartment of Psychiatry, Roozbeh Hospital
hIranian National Center for Addiction Studies, Tehran University of Medical Sciences;
dJanbazan Medical and Engineering Research Center
fDepartment of Psychiatry, Iran University of Medical Center, Tehran, Iran
gDepartment of Medicine (Biomedical Genetics), Boston University School of Medicine, Boston, Massachusetts, USA
* Hamid Mostafavi-Abdolmaleky and Mohammad Reza Zarindast contributed equally and co-directed this work.
Received 2 March 2019 Accepted 13 August 2019
Correspondence to Mohammad Reza Zarindast, Department of Pharmacology, School of Medicine, Tehran university of Medical Sciences, Tehran, Iran, Tel: +9821 6640 2569; fax: +9821 6640 2569; e-mail: email@example.com