Suchergebnisse

AbstractInhibitory control is widely hypothesized to be the cornerstone of executive function in childhood and the central deficit in a number of developmental disorders, including attention‐deficit/hyperactivity disorder (ADHD). However, recent evidence from adults indicates that performance on response inhibition tasks may primarily reflect non‐inhibitory attentional control (context monitoring) processes. Yet it may be that inhibition plays a more central role in childhood – a time when the architecture of cognitive processes might be more transparent due to wide variability in skill level. Here we directly test inhibitory and context monitoring explanations of task performance on a Go/No‐Go task in a large group of children 4–12 years of age. We conclude that traditional inhibitory conceptualizations of task performance on the Go/No‐Go task cannot account for our findings, calling into question evidence supporting a central role for inhibitory control in cognitive development or developmental psychopathology.

AbstractLow socioeconomic status (SES) is associated with greater risk for symptoms of attention‐deficit/hyperactivity disorder (ADHD). One mechanism through which SES may confer risk for ADHD is by influencing brain structure. Alterations to cortical thickness, surface area and subcortical volume have been associated with low SES and with the presence of ADHD across multiple studies. The current study examined whether cortical thickness, surface area or subcortical volume mediate the associations between SES and ADHD in youth 3–21 years old (N = 874) from the Pediatric Imaging, Neurocognition and Genetics Study. Freesurfer was used to estimate cortical thickness, surface area and subcortical volume from structural magnetic resonance imaging. Parents reported on demographics, family SES, ADHD diagnoses and the presence of child attention problems. Statistical mediation was assessed using a bootstrap resampling procedure. Controlling for parental ADHD, child age, gender, birth weight and scanner, children in low SES families were more likely to be in the ADHD group. Consistent with previous reports in this sample, low SES was associated with reduced surface area across the frontal lobe and reduced subcortical volume in the amygdala, cerebellum, hippocampus and basal ganglia. Of these regions, a significant indirect effect of SES on ADHD status through subcortical volume was observed for the left cerebellum (95% confidence interval: 0.004, 0.022), the right cerebellum (95% confidence interval: 0.006, 0.025), and the right caudate (95% confidence interval: 0.002, 0.022). Environmentally mediated changes in the cerebellum and the caudate may be neurodevelopmental mechanisms explaining elevated risk of ADHD in children in low SES families.

We show that a number of noncognitive skills and preferences, including patience and identity, are malleable in adults, and that investments in them reduce crime and violence. We recruited criminally engaged men and randomized one-half to eight weeks of cognitive behavioral therapy designed to foster self-regulation, patience, and a noncriminal identity and lifestyle. We also randomized $200 grants. Cash alone and therapy alone initially reduced crime and violence, but effects dissipated over time. When cash followed therapy, crime and violence decreased dramatically for at least a year. We hypothesize that cash reinforced therapy's impacts by prolonging learning-by-doing, lifestyle changes, and self-investment. (JEL D12, D83, H23, I32, K42, O15, O17)

Adverse childhood experiences have been associated with more negative coupling between the ventromedial prefrontal cortex (vmPFC) and amygdala, a brain network involved in emotion regulation in both children and adults. This pattern may be particularly likely to emerge in individuals exposed to threatening experiences during childhood (e.g., exposure to child abuse), although this has not been examined in prior research. We collected functional magnetic resonance imaging data on 57 adolescents during an emotion regulation task. Greater negative functional connectivity between vmPFC and amygdala occurred during viewing of negative compared to neutral images. This vmPFC-amygdala task-related functional connectivity was more negative in adolescents exposed to physical, sexual, or emotional abuse than those without a history of maltreatment and was associated with abuse severity. This pattern of more negative functional connectivity was associated with higher levels of externalizing psychopathology concurrently and 2 years later. Greater negative connectivity in the vmPFC-amygdala network during passive viewing of negative images may reflect disengagement of regulatory responses from vmPFC in situations eliciting strong amygdala reactivity, potentially due to stronger appraisals of threat in children exposed to early threatening environments. This pattern may be adaptive in the short term but place adolescents at higher risk of psychopathology later in life.

AbstractThe association of parental social status with multiple health and achievement indicators in adulthood has driven researchers to attempt to identify mechanisms by which social experience in childhood could shift developmental trajectories. Some accounts for observed linkages between parental social status in childhood and health have hypothesized that early stress exposure could result in chronic disruptions in hypothalamic‐pituitary‐adrenal (HPA) axis activation, and that this activation could lead to long‐term changes. A robust literature in adult animals has demonstrated that chronic HPA axis activation leads to changes in hippocampal structure and function. In the current study, consistent with studies in animals, we observe an association between both maternal self‐rated social status and hippocampal activation in children and between maternal self‐rated social status and salivary cortisol in children.

AbstractExposure to childhood adversity is common and associated with a host of negative developmental outcomes. The most common approach used to examine the consequences of adversity exposure is a cumulative risk model. Recently, we have proposed a novel approach, the dimensional model of adversity and psychopathology (DMAP), where different dimensions of adversity are hypothesized to impact health and well‐being through different pathways. We expect deprivation to primarily disrupt cognitive processing, whereas we expect threat to primarily alter emotional reactivity and automatic regulation. Recent hypothesis‐driven approaches provide support for these differential associations of deprivation and threat on developmental outcomes. However, it is not clear whether these patterns would emerge using data‐driven approaches. Here we use a network analytic approach to identify clusters of related adversity exposures and outcomes in an initial study (Study 1: N = 277 adolescents aged 16–17 years; 55.1% female) and a replication (Study 2: N = 262 children aged 8–16 years; 45.4% female). We statistically compare our observed clusters with our hypothesized DMAP model and a clustering we hypothesize would be the result of a cumulative stress model. In both samples we observed a network structure consistent with the DMAP model and statistically different than the hypothesized cumulative stress model. Future work seeking to identify in the pathways through which adversity impacts development should consider multiple dimensions of adversity.