Early deprivation disruption of associative learning is a developmental pathway to depression and social problems.

Exposure to psychosocial deprivation is associated with elevations in numerous forms of impairment throughout the life-course. Disruptions in associative learning may be a key mechanism through which adversity, particularly psychosocial deprivation, increases risk for impairment. Existing data consistent with this claim come entirely from correlational studies. Here, we present the first experimental evidence relating psychosocial deprivation and disruptions in multiple forms of associative learning. Using data from the Bucharest Early Intervention Project, we demonstrate that randomized placement into a family caregiving environment during the infant/toddler period as compared to prolonged institutional care normalizes two forms of associative learning in early adolescence: reward responsivity and implicit motor learning. These forms of associative learning significantly mediate the effect of institutional rearing on depressive symptoms and peer relationships. In sum, we provide evidence for a novel pathway linking early experience to psychopathology and peer relationships through basic associative learning mechanisms.

As Working Memory Grows: A Developmental Account of Neural Bases of Working Memory Capacity in 5- to 8-Year Old Children and Adults.

Working memory develops slowly: Even by age 8, children are able to maintain only half the number of items that adults can remember. Neural substrates that support performance on working memory tasks also have a slow developmental trajectory and typically activate to a lesser extent in children, relative to adults. Little is known about why younger participants elicit less neural activation. This may be due to maturational differences, differences in behavioral performance, or both. Here we investigate the neural correlates of working memory capacity in children (ages 5-8) and adults using a visual working memory task with parametrically increasing loads (from one to four items) using fMRI. This task allowed us to estimate working memory capacity limit for each group. We found that both age groups increased the activation of frontoparietal networks with increasing working memory loads, until working memory capacity was reached. Because children's working memory capacity limit was half of that for adults, the plateau occurred at lower loads for children. Had a parametric increase in load not been used, this would have given an impression of less activation overall and less load-dependent activation for children relative to adults. Our findings suggest that young children and adults recruit similar frontoparietal networks at working memory loads that do not exceed capacity and highlight the need to consider behavioral performance differences when interpreting developmental differences in neural activation.

Previous reward decreases errors of commission on later 'No-Go' trials in children 4 to 12 years of age: evidence for a context monitoring account.

Inhibitory 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.

Widespread reductions in cortical thickness following severe early-life deprivation: a neurodevelopmental pathway to attention-deficit/hyperactivity disorder.

BACKGROUND: Children exposed to early-life psychosocial deprivation associated with institutional rearing are at markedly elevated risk of developing attention-deficit/hyperactivity disorder (ADHD). Neurodevelopmental mechanisms that explain the high prevalence of ADHD in children exposed to institutionalization are unknown. We examined whether abnormalities in cortical thickness and subcortical volume were mechanisms explaining elevations in ADHD among children raised in institutional settings. METHODS: Data were drawn from the Bucharest Early Intervention Project, a cohort of children raised from early infancy in institutions in Romania (n = 58) and age-matched community control subjects (n = 22). Magnetic resonance imaging data were acquired when children were aged 8 to 10 years, and ADHD symptoms were assessed using the Health and Behavior Questionnaire. RESULTS: Children reared in institutions exhibited widespread reductions in cortical thickness across prefrontal, parietal, and temporal regions relative to community control subjects. No group differences were found in the volume of subcortical structures. Reduced thickness across numerous cortical areas was associated with higher levels of ADHD symptoms. Cortical thickness in lateral orbitofrontal cortex, insula, inferior parietal cortex, precuneus, superior temporal cortex, and lingual gyrus mediated the association of institutionalization with inattention and impulsivity; additionally, supramarginal gyrus thickness mediated the association with inattention and fusiform gyrus thickness mediated the association with impulsivity. CONCLUSIONS: Severe early-life deprivation disrupts cortical development resulting in reduced thickness in regions with atypical function during attention tasks in children with ADHD, including the inferior parietal cortex, precuneus, and superior temporal cortex. These reductions in thickness are a neurodevelopmental mechanism explaining elevated ADHD symptoms in children exposed to institutional rearing.