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BACKGROUND:Childhood maltreatment is one of the most potent predictors of future psychopathology, including internalizing disorders. It remains unclear whether heightened amygdala reactivity to threat and elevated stress exposure may be implicated in the pathogenesis and maintenance of internalizing disorders among individuals with a history of childhood maltreatment. METHODS:Using data from a sample of 1,144 young adults, we investigated the contribution of baseline threat-related amygdala reactivity and prospective major stressful life events to internalizing symptoms severity 1 year later (on average) in individuals with a history of maltreatment (n = 100) and propensity score matched nonmaltreated peers (n = 96). RESULTS:Even after stringently matching for several potentially confounding variables - including baseline internalizing symptoms, socioeconomic status and IQ - childhood maltreatment status predicted increased amygdala reactivity at baseline, elevated post-baseline exposure to major stressful life events and internalizing symptoms at follow-up. We also showed, for the first time, that amygdala reactivity at baseline and also post-baseline exposure to major stressful life events mediated the association between a history of maltreatment and future internalizing symptoms. CONCLUSIONS:These findings provide support for the view that maltreatment is a potent developmental insult leading to long-lasting neurocognitive recalibrations of the threat processing system. It is possible that such alterations, over time, may impact mental health functioning by compromising the ability to effectively negotiate everyday challenges (stress susceptibility). These alterations were not, however, found to sensitize an individual to the impact of major stressful life events. The results of this study also lend compelling support to the view that increased psychiatric risk, in the context of childhood maltreatment, follows from an increased propensity to experience major stressful life events (stress generation).

Background: Prosocial behaviours – acts that benefit others – are of crucial importance for many species including humans. However, adolescents with conduct problems (CP), unlike their typically developing (TD) peers, demonstrate markedly reduced engagement in prosocial behaviours. This pattern is particularly pronounced in adolescents with CP and high levels of callous‐unemotional traits (CP/HCU) who are at increased risk of developing psychopathy in adulthood. While a substantial amount of research has investigated the cognitive‐affective mechanisms thought to underlie antisocial behaviour, much less is known about the mechanisms that could explain reduced prosocial behaviours in adolescents with CP. Methods: Here we examined the willingness to exert effort to benefit oneself (self) and another person (other, prosocial condition) in children with CP/HCU, CP and lower levels of CU traits (CP/LCU) and their TD peers. The task captured both prosocial choices, and actual effort exerted following prosocial choices, in adolescent boys aged 11–16 (27 CP/HCU; 34 CP/LCU; 33 TD). We used computational modelling to reveal the mechanistic processes involved when choosing prosocial acts. Results: We found that both CP/HCU and CP/LCU groups were more averse to initiating effortful prosocial acts than TD adolescents – both at a cognitive and at a behavioural level. Strikingly, even if they chose to initiate a prosocial act, the CP/HCU group exerted less effort following this prosocial choice than other groups. Conclusions: Our findings indicate that reduced exertion of effort to benefit others may be an important factor that differentiates adolescents with CP/HCU from their peers with CP/LCU. They offer new insights into what might drive low prosocial behaviour in adolescents with CP, including vulnerabilities that may particularly characterise those with high levels of CU traits. [ABSTRACT FROM AUTHOR]

Background: Schizophrenia is a neurodevelopmental disorder, and risk genes are thought to act through disruption of brain development. Several genetic studies have identified dystrobrevin-binding protein 1 (DTNBP1, also known as dysbindin) as a potential susceptibility gene for schizophrenia, but its impact on brain development is poorly understood. The present investigation examined for the first time the effects of DTNBP1 on brain structure in children. Our hypothesis was that a genetic variation in DTNBP1 (i.e., the single nucleotide polymorphism rs2619538) would be associated with differences in both gray and white matter brain regions previously implicated in schizophrenia. Methods: Magnetic resonance imaging and voxel-based morphometry were used to examine brain structure in 52 male children aged between 10 and 12 years. Statistical inferences on the effects of DTNBP1 genotype on gray and white matter volume (GMV and WMV) were made at p less than 0.05 after family-wise error correction for multiple comparisons across the whole brain. Results: Individuals homozygous for the schizophrenia high-risk allele (AA) compared with those homozygous for the low-risk allele (TT) expressed reduced GMV in the left anterior cingulate gyrus and reduced WMV in the left medial frontal area. Conclusions: Our results suggest that genetic variation in DTNBP1 is associated with differences in gray and white matter; and that these effects are already evident in children as young as 10-12 years. These findings are consistent with the notion that the DTNBP1 genotype influences brain development and may thereby modulate vulnerability to schizophrenia.

Objective: To investigate the longitudinal development of callous-unemotional traits (CU) in middle childhood using developmental trajectory analyses in a large twin dataset and examine the degree to which genetic and environmental influences contributed to the CU trajectory-group membership in children. Method: The study included 9,462 youths from the Twins Early Development Study, a population-based sample of twins from the United Kingdom. Developmental trajectories were described using teachers' ratings of CU at 7, 9, and 12 years old. Results: We identified four trajectories of CU through general growth mixture modeling: stable high, increasing, decreasing, and stable low. In most cases, the trajectory-group membership was largely driven by genetic and to a lesser extent by nonshared environmental influences for boys and girls. The most notable exception was a strong contribution of shared environment for the girls in the stable-high trajectory group. Conclusions: Our findings suggest distinct developmental trajectories of CU from childhood to early adolescence, which are in most cases influenced by genetic factors and, to a lesser degree, by nonshared environmental factors. Highest heritability was observed for boys on a stable-high CU trajectory. Interestingly, the trajectory-group membership for girls on a stable-high CU trajectory appeared to be almost entirely driven by shared environmental influences. These differences in the etiology of stable-high CU in boys and girls have potential implications for clinical practice and studies attempting to identify genetic and environmental risk factors for high CU. (Contains 1 figure and 4 tables.)

Objectives: Childhood maltreatment is associated with altered neural reactivity during autobiographical memory (ABM) recall and a pattern of overgeneral memory (OGM). Altered ABM and OGM have been linked with psychopathology and poorer social functioning. The present study investigated the association between altered ABM and subsequent socio-emotional functioning (measured two years later) in a sample of adolescents with (N = 20; maltreatment group, MT) and without (N = 17; non-MT group) documented childhood maltreatment histories. Method: At baseline, adolescents (aged 12.6 ± 1.45 years) were administered the Autobiographical Memory Test to measure OGM. Participants also recalled specific ABMs in response to emotionally valenced cue words during functional MRI. Adolescents in both groups underwent assessments measuring depressive symptoms and prosocial behavior at both timepoints. Regression analyses were carried out to predict outcome measures at follow-up controlling for baseline levels. Results: In the MT group, greater OGM at baseline significantly predicted reduced prosocial behavior at follow-up and showed a trend level association with elevated depressive symptoms. Patterns of altered ABM-related brain activity did not significantly predict future psycho-social functioning. Conclusions: The current findings highlight the potential value of OGM as a cognitive mechanism that could be targeted to reduce risk of depression in adolescents with prior histories of maltreatment. [ABSTRACT FROM AUTHOR]

There is a well-established association between childhood maltreatment and later poor mental health and increasing recognition that we need to find ways to support children following such experiences to improve long-term outcomes. We suggest that the rationale for such a preventive approach is directly informed by the emerging findings from the field of functional neuroimaging. Here, we review the evidence from four neurocognitive systems: threat processing, reward processing, emotion regulation and executive control. We briefly summarise what is known about each system, review the evidence that altered functioning is implicated in common mental health problems and describe how the functioning of each system is altered following maltreatment. Across domains, these neurocognitive alterations following child maltreatment are in line with those seen in adults presenting with mental health problems yet most maltreated children studied do not have a presenting 'disorder'. This suggests that these neurocognitive alterations may potentiate the risk of future psychopathology. We discuss this possibility in the context of the theory of latent vulnerability (McCrory and Viding, 2015). According to this model, children may respond to early adverse environments in ways that are potentially adaptive in the short term but which create vulnerability to future mental health problems in the long term. We also consider the clinical implications of the neuroimaging evidence ‒ in particular, the growing need for a more preventive clinical approach. [ABSTRACT FROM AUTHOR]