7 research outputs found

    A biomarker of brain arousal mediates the intergenerational link between maternal and child post-traumatic stress disorder.

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    This study examined whether there is a biological basis in the child's resting brain activity for the intergenerational link between maternal interpersonal violence-related posttraumatic stress disorder (IPV-PTSD) and child subclinical symptoms. We used high-density EEG recordings to investigate the resting brain activity in a sample of 57 children, 34 from mothers with IPV-PTSD, and 23 from mothers without PTSD. These children were part of a prospective, longitudinal study focusing on the offspring of mothers with and without IPV-PTSD, reporting how the severity of a mother's IPV-PTSD can impact her child's emotional regulation and risk for developing mental illness. However, we had not yet looked into potential EEG biomarkers during resting state that might mediate and/or moderate effects of maternal IPV-PTSD severity on child mental health, and in particular the risk for PTSD. The alpha band spectral power as well as the aperiodic exponent of the power spectrum (PLE; power-law exponent) were examined as mediators of maternal IPV-PTSD and child PTSD. While there was no difference in alpha spectral power between the two groups, PLE was significantly reduced in children of mothers with IPV-PTSD compared to control children, indicating cortical hyper-arousal. Interestingly, child PLE was negatively correlated with the severity of maternal IPV-PTSD, suggesting an intergenerational interaction. This interpretation was reinforced by a negative correlation between child PLE and child PTSD symptoms. Finally, causal analyses using structural equation modelling indicated that child PLE mediated the relationship between maternal PTSD severity and child PTSD. Our observations suggest that maternal IPV-PTSD has an intergenerational impact on the child neurobehavioral development through a correlated abnormal marker of brain arousal (i.e. child PLE). These findings are potentially relevant to psychotherapy research and to the development of more effective psycho-neurobehavioral therapies (i.e. neurofeedback) among affected individuals

    The association of serotonin receptor 3A methylation with maternal violence exposure, neural activity, and child aggression

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    Background Methylation of the serotonin 3A receptor gene (HTR3A) has been linked to child maltreatment and adult psychopathology. The present study examined whether HTR3A methylation might be associated with mothers' lifetime exposure to interpersonal violence (IPV), IPV-related psychopathology, child disturbance of attachment, and maternal neural activity. Methods Number of maternal lifetime IPV exposures and measures of maternal psychopathology including posttraumatic stress disorder (PTSD), major depression and aggressive behavior (AgB), and a measure of child attachment disturbance known as “secure base distortion” (SBD) were assessed in a sample of 35 mothers and children aged 12–42 months. Brain fMRI activation was assessed in mothers using 30-s silent film excerpts depicting menacing adult male-female interactions versus prosocial and neutral interactions. Group and continuous analyses were performed to test for associations between clinical and fMRI variables with DNA methylation. Results Maternal IPV exposure-frequency was associated with maternal PTSD; and maternal IPV-PTSD was in turn associated with child SBD. Methylation status of several CpG sites in the HTR3A gene was associated with maternal IPV and IPV-PTSD severity, AgB and child SBD, in particular, self-endangering behavior. Methylation status at a specific CpG site (CpG2_III) was associated with decreased medial prefrontal cortical (mPFC) activity in response to film-stimuli of adult male-female interactions evocative of violence as compared to prosocial and neutral interactions. Conclusions Methylation status of the HTR3A gene in mothers is linked to maternal IPV-related psychopathology, trauma-induced brain activation patterns, and child attachment disturbance in the form of SBD during a sensitive period in the development of self-regulation
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