Abstract
There is great body of evidence showing a relationship between childhood adversity and psychosis onset. Genetic factors moderate the association between childhood adversity and psychosis risk potentially by influencing biological and/or psychological reaction following exposure to adversity. In this review, we discuss studies identifying the specific genetic variants known to affect dopamine levels involved in this interaction. Our review shows that the catechol-O-methyltransferase (COMT), dopamine D2 receptor (DRD2), AKT1 gene play a key role in mediating the relationship between childhood adversity and development of psychosis. We have also found conflicting findings on the impact of dopamine genes on the relationship between childhood adversity and development of psychosis, suggesting that other genetic and environmental factors should be taken into account. We here discuss the implications of our findings and future directions.
Highlights
The dopamine hypothesis of schizophrenia is the leading and longest standing theory of schizophrenia pathophysiology, stating that characteristic symptoms such as hallucinations, delusions and abnormal cognitive functioning are caused by a synergistic imbalance of dopamine neurotransmission in cortical and subcortical brain regions (Howes & Kapur, 2009; Kimura et al, 2021; Takao et al, 2021)
Childhood trauma and other types of stressful experiences are well established as a significant risk factor for the development of psychosis (Janssen et al, 2004; Kessler et al, 2010; Matheson et al, 2013; Read et al, 2009; Varese et al, 2012)
A history of childhood trauma has been shown to be more frequent in individuals at ultra-high risk (UHR) of psychosis (Kraan, van Dam, et al, 2015; Kraan, Velthorst, et al, 2015), individuals with psychotic-like experiencing (Boyda & McFeeters, 2015; 1 3 Vol.:(0123456789)
Summary
The dopamine hypothesis of schizophrenia is the leading and longest standing theory of schizophrenia pathophysiology, stating that characteristic symptoms such as hallucinations, delusions and abnormal cognitive functioning are caused by a synergistic imbalance of dopamine neurotransmission in cortical and subcortical brain regions (Howes & Kapur, 2009; Kimura et al, 2021; Takao et al, 2021). There was a gene-environment interaction among healthy young men during a semi-experimental stress exposure showing individuals with the Val allele having increased level of psychotic symptoms in comparison with the Met homozygotes (Stefanis et al, 2007); future studies should investigate whether the same results hold true fo female participants.
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