Abstract
Both childhood trauma and a functional catechol-O-methyltransferase (COMT) genetic polymorphism have been associated with posttraumatic stress disorder (PTSD) and depression; however, it is still unclear whether the two interact and how this interaction relates to long-term risk or resilience. Imaging and genotype data were collected on 73 highly traumatized women. DNA extracted from saliva was used to determine COMT genotype (Val/Val, n = 38, Met carriers, n = 35). Functional MRI data were collected during a Go/NoGo task to investigate the neurocircuitry underlying response inhibition. Self-report measures of adult and childhood trauma exposure, PTSD and depression symptom severity, and resilience were collected. Childhood trauma was found to interact with COMT genotype to impact inhibition-related hippocampal activation. In Met carriers, more childhood trauma was associated with decreased hippocampal activation, whereas in the Val/Val group childhood trauma was related to increased hippocampal activation. Second, hippocampal activation correlated negatively with PTSD and depression symptoms and positively with trait resilience. Moreover, hippocampal activation mediated the relationship between childhood trauma and psychiatric risk or resilience in the Val/Val, but not in the Met carrier group. These data reveal a potential mechanism by which childhood trauma and COMT genotype interact to increase risk for trauma-related psychopathology or resilience. Hippocampal recruitment during inhibition may improve the ability to use contextual information to guide behavior, thereby enhancing resilience in trauma-exposed individuals. This finding may contribute to early identification of individuals at risk and suggests a mechanism that can be targeted in future studies aiming to prevent or limit negative outcomes.
Highlights
Trauma exposure during childhood is a well-known risk factor for later development of psychiatric disorders, such as posttraumatic stress disorder (PTSD) and depression [1]
The two genotype groups did not differ in age, behavioral task performance, adult trauma load, childhood trauma, PTSD or depression symptoms, and resilience (Table 1)
We demonstrated that childhood trauma and the presence of the Met allele was associated with decreased inhibition-related hippocampal activation, whereas childhood trauma in the Val/Val group was related to increased activation in the hippocampus
Summary
Trauma exposure during childhood is a well-known risk factor for later development of psychiatric disorders, such as posttraumatic stress disorder (PTSD) and depression [1]. It is possible that polymorphisms of this gene affect brain structure, function, or related cognitive processes following exposure to trauma These neural and cognitive changes may in turn, increase the likelihood for developing psychopathology or enhance resilience. We recently observed an association between childhood trauma and decreased inhibition-related rACC activation in adults with PTSD, but not in a traumatized control group [35] This evidence suggests that childhood trauma impacts inhibition-related brain processes, not in all individuals exposed to early trauma, pointing to a potential risk mechanism for childhood trauma-related psychopathology. We hypothesized that more childhood trauma is associated with decreased inhibition-related activation in the vmPFC and hippocampus only in the risk (Met carrier) group and with more vmPFC and hippocampal activation in the Val/Val group. As volumetric measures of the hippocampus showed differences for left and right in PTSD [20], we analyzed the left and right hippocampus separately
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