Research into phenotype–genotype correlations in neurodevelopmental disorders has greatly elucidated the contribution of genetic and neurobiological factors to variations in typical and atypical development. Etiologically relatively homogeneous disorders, such as Williams syndrome (WS), provide unique opportunities for elucidating gene–brain–behavior relationships. WS is a neurogenetic disorder caused by a hemizygous deletion of approximately 25 genes on chromosome 7q11.23. This results in a cascade of physical, cognitive–behavioral, affective, and neurobiological aberrations. WS is associated with a markedly uneven neurocognitive profile, and the mature state cognitive profile of WS is relatively well developed. Although anecdotally, individuals with WS have been frequently described as unusually friendly and sociable, personality remains a considerably less well studied area. This paper investigates genetic influences, cognitive–behavioral characteristics, aberrations in brain structure and function, and environmental and biological variables that influence the social outcomes of individuals with WS. We bring together a series of findings across multiple levels of scientific enquiry to examine the social phenotype in WS, reflecting the journey from gene to the brain to behavior. Understanding the complex multilevel scientific perspective in WS has implications for understanding typical social development by identifying important developmental events and markers, as well as helping to define the boundaries of psychopathology.

Temperament, effortful control, and problem behaviors at 4.5 years were assessed in 72 children classified as exuberant, inhibited, and low reactive as 2-year-olds. Exuberant toddlers were more positive, socially responsive to novel persons, less shy, and rated as having more problem behaviors, including externalizing and internalizing behaviors, than other children as preschoolers. Two forms of effortful control, the ability to delay a response and the ability to produce a subdominant response, were associated with fewer externalizing behaviors, whereas expressing more negative affect (relative to positive/neutral affect) when disappointed was related to more internalizing behaviors. Interaction effects implicated high levels of unregulated emotion during disappointment as a risk factor for problem behaviors in exuberant children.

Most contemporary accounts of psychopathology acknowledge the importance of both biological and environmental influences on behavior. In developmental psychopathology, multiple etiological mechanisms for psychiatric disturbance are well recognized, including those operating at genetic, neurobiological, and environmental levels of analysis. However, neuroscientific principles are rarely considered in current approaches to prevention or intervention. In this article, we explain why a deeper understanding of the genetic and neural substrates of behavior is essential for the next generation of preventive interventions, and we outline 10 specific reasons why considering biological processes can improve treatment efficacy. Among these, we discuss (a) the role of biomarkers and endophenotypes in identifying those most in need of prevention; (b) implications for treatment of genetic and neural mechanisms of homotypic comorbidity, heterotypic comorbidity, and heterotypic continuity; (c) ways in which biological vulnerabilities moderate the effects of environmental experience; (d) situations in which Biology × Environment interactions account for more variance in key outcomes than main effects; and (e) sensitivity of neural systems, via epigenesis, programming, and neural plasticity, to environmental moderation across the life span. For each of the 10 reasons outlined we present an example from current literature and discuss critical implications for prevention.

Children (N = 324 boys, 315 girls) between the ages of 2.5 and 6 (mean age = 3.63) were identified in a house to house survey in low-income areas (income <20th percentile nationally) of urban Mexico. The Center for Epidemiologic Studies—Depression Scale was administered to mothers of all children. Salivary cortisol samples were taken in children as a measure of hypothalamic–pituitary–adrenocortical (HPA) system activity at time of arrival (baseline, Time 0), 25 min after arrival (Time 1), and 50 min after arrival (Time 2). Between Time 0 and Time 1, children were administered several cognitive tests. Results of hierarchical linear modeling analyses revealed that higher levels of maternal depressive symptoms were associated with lower baseline cortisol levels in their children (p < .05), while controlling for age, gender, and time since awakening. Higher levels of maternal depressive symptoms were associated with less of an increase in salivary cortisol to the arrival of the experimenters and subsequent cognitive testing (p < .05). All results were moderated by gender, with enhanced cortisol response in girls and no response in boys. These results suggest that among very low-income families, high maternal depressive symptoms are associated with hypoactivity of the HPA system in children, particularly boys.

The degree to which infant attention behaviors, together with infant reactivity to frustrating events, predict aggressive behavior at 2.5 years, and the moderating effect of maternal behavior were tested with 64 low-risk mothers and infants. Mothers rated infant negative reactivity at 5 months and aggressive behavior and maternal trait anger at 2.5 years; infant and maternal behaviors were observed at 6 months. Based on hierarchical multiple regressions, infant attention to frustrating events at 6 months positively predicted aggressive behavior, whereas looking away from frustrating events was associated with less aggressive behavior for girls only. High reactivity to limits predicted aggressive behavior only when mothers encouraged infant attention to the frustrating event, suggesting that maternal behavior amplifies developmental pathways associated with infant temperament.

Structural and functional magnetic resonance imaging (MRI) are increasingly common research methods among investigators interested in typically and atypically developing populations. However, the effective use of these tools requires an understanding of the basis of the magnetic resonance signal, as well as some of the additional experimental complications that arise when collecting MRI data from developmental populations. This primer provides a foundation for investigators who wish to utilize MRI methods in their research and whose primary interest involves typically and atypically developing populations. The basic concepts of MRI physics are introduced, as well as the typical MRI scanner components and their role in MRI data acquisition. In addition, a variety of scan types (structural, functional, diffusion tensor) are discussed, along with a number of important experimental design factors that can impact the quality and utility of the data collected. Special consideration is given to working with pediatric and special populations.

The psychological construct of empathy refers to an intersubjective induction process by which positive and negative emotions are shared, without losing sight of whose feelings belong to whom. Empathy can lead to personal distress or to empathic concern (sympathy). The goal of this paper is to address the underlying cognitive processes and their neural underpinnings that constitute empathy within a developmental neuroscience perspective. In addition, we focus on how these processes go awry in developmental disorders marked by impairments in social cognition, such as autism spectrum disorder, and conduct disorder. We argue that empathy involves both bottom-up and top-down information processing, underpinned by specific and interacting neural systems. We discuss data from developmental psychology as well as cognitive neuroscience in support of such a model, and highlight the impact of neural dysfunctions on social cognitive developmental behavior. Altogether, bridging developmental science and cognitive neuroscience helps approach a more complete understanding of social cognition. Synthesizing these two domains also contributes to a better characterization of developmental psychopathologies that impacts the development of effective treatment strategies.

This study investigated joint effects of maternal prenatal smoking and parental history of antisocial behavior on physical aggression between ages 17 and 42 months in a population sample of children born in Québec (N = 1,745). An analysis of variance (ANOVA) showed significant main effects of maternal prenatal smoking and a significant interaction between maternal prenatal smoking and mother's history of antisocial behavior in the prediction of children's probability to display high and rising physical aggression. The interaction indicated that the effects of heavy smoking during pregnancy (≥10 cigarettes/day) were greater when the mother also had a serious history of antisocial behavior. The effects remained significant after the introduction of control variables (e.g., hostile-reactive parenting, family functioning, parental separation/divorce, family income, and maternal education). Another significant interaction not accounted for by control variables was observed for maternal prenatal smoking and family income, indicating more serious effects of maternal prenatal smoking under relatively low-income, conditions. Both interactions indicate critical adversities that, in combination with maternal prenatal smoking, have supra-additive effects on (the development of) physical aggression during early childhood. These findings may have implications for the selection of intervention targets and strategies.

This study examines the relation between the longitudinal course of maternal depression during the child's early life and children's psychophysiology and behavior at age 6.5 years. One hundred fifty-nine children of depressed and nondepressed mothers were followed from infancy through age 6.5 years. Growth mixture modeling was used to identify classes of depressed mothers based on the longitudinal course of the mother's depression. School-aged children of chronically depressed mothers were found to have elevated externalizing behavior problems, decreased social competence, reduced frontal brain activation (EEG power), and higher respiratory sinus arrhythmia reactivity. Children of mothers with decreasing and stable mild depression were found to have increased hyperactivity and attention problems compared to children of nondepressed mothers. Contextual risk factors were found to mediate the relation between maternal depression and child behavioral outcomes.

Advances in the fields of cognitive and affective developmental neuroscience, developmental psychopathology, neurobiology, genetics, and applied behavior analysis have contributed to a more optimistic outcome for individuals with autism spectrum disorder (ASD). These advances have led to new methods for early detection and more effective treatments. For the first time, prevention of ASD is plausible. Prevention will entail detecting infants at risk before the full syndrome is present and implementing treatments designed to alter the course of early behavioral and brain development. This article describes a developmental model of risk, risk processes, symptom emergence, and adaptation in ASD that offers a framework for understanding early brain plasticity in ASD and its role in prevention of the disorder.

Although peer victimization places children at serious risk for aggressive behavior, not all victimized children are aggressive. The diathesis–stress hypothesis of disease proposes that an environmental stressor such as peer victimization should to lead to maladjustment mostly in those individuals with preexisting genetic vulnerabilities. Accordingly, this study examined whether the link between peer victimization and child aggression is moderated by children's genetic risk for such behavior. Using a sample of 506 6-year-old twins, peer victimization was assessed through peer nominations and aggressive behavior was assessed through peer and teacher reports. Children's genetic risk for aggression was estimated as a function of their co-twin's aggression and the pair's zygosity. Genetic modeling showed that peer victimization is an environmentally driven variable that is unrelated to children's genetic disposition. Results also provided support for the notion of a gene–environment interaction between peer victimization and child's genetic risk for aggressive behavior, albeit only in girls. For boys, peer victimization was related to aggression regardless of the child's genetic risk for such behavior. Different socialization experiences in girls' compared to boys' peer groups may explain the different pattern of results for girls and boys.

Children with autism are developmentally delayed in following the direction of another person's gaze in social situations. A number of studies have measured reflexive orienting to eye gaze cues using Posner-style laboratory tasks in children with autism. Some studies observe normal patterns of cueing, suggesting that children with autism are alert to the significance of the eyes, whereas other studies reveal an atypical pattern of cueing. We review this contradictive evidence to consider the extent to which sensitivity to gaze is normal, and ask whether apparently normal performance may be a consequence of atypical (nonsocial) mechanisms. Our review concludes by highlighting the importance of adopting a developmental perspective if we are to understand the reasons why people with autism process eye gaze information atypically.

We describe recent progress in our program of research that aims to use functional magnetic resonance imaging (fMRI) to identify and delineate the brain systems involved in social perception and to chart the development of those systems and their roles as mechanisms supporting the development of social cognition in children, adolescents, and adults with and without autism. This research program was initiated with the intention of further specifying the role of the posterior superior temporal sulcus (STS) region in the network of neuroanatomical structures comprising the social brain. Initially, this work focused on evaluating STS function when typically developing adults were engaged in the visual analysis of other people's actions and intentions. We concluded that that the STS region plays an important role in social perception via its involvement in representing and predicting the actions and social intentions of other people from an analysis of biological–motion cues. These studies of typically developing people provided a set of core findings and a methodological approach that informed a set of fMRI studies of social perception dysfunction in autism. The work has established that dysfunction in the STS region, as well as reduced connectivity between this region and other social brain structures including the fusiform gyrus and amygdala, play a role in the pathophysiology of social perception deficits in autism. Most recently, this research program has incorporated a developmental perspective in beginning to chart the development of the STS region in children with and without autism.

The effect of the Video-Feedback Intervention to Promote Positive Parenting and Sensitive Discipline (VIPP-SD) on daily cortisol production was tested in a randomized controlled trial with 130 families with 1- to 3-year-old children screened for their relatively high levels of externalizing behavior. Six 1.5-hr intervention sessions focusing on maternal sensitivity and discipline were conducted with individual families at their homes. Children in the intervention group showed lower cortisol levels, with a moderating role of the dopamine receptor D4 (DRD4) VNTR exon III polymorphism. The VIPP-SD program proved to be effective in decreasing daily cortisol production in children with the DRD4 7-repeat allele, but not in children without the DRD4 7-repeat allele. Our findings indicate that children are differentially susceptible to intervention effects dependent on the presence of the 7-repeat DRD4 allele.

We investigated narratives, symbolic play, and emotions in children who varied in severity of disruptive behavior problems. Children's representations of hypothetical situations of conflict and distress were assessed at 4–5 and 7 years. Behavior problems also were assessed then and again at 9 years. Children's aggressive and caring themes differentiated nonproblem children, children whose problems remained or worsened with age, and those whose problems improved over time. Differences in boys and girls whose problems continued sometimes reflected exaggerations of prototypic gender differences seen across the groups. Boys with problems showed more hostile themes (physical aggression and anger), whereas girls with problems showed more caring (prosocial) themes relative to the other groups. Modulated (verbal) aggression, more common in girls than boys, showed developmentally appropriate increases with age. However, this was true only for children without problems and those whose problems improved. We consider how these findings contribute to an understanding the inner worlds of boys and girls who differ in their early developmental trajectories for behavior problems.

Despite their potentially central role in fostering school readiness, executive function (EF) skills have received little explicit attention in the design and evaluation of school readiness interventions for socioeconomically disadvantaged children. The present study examined a set of five EF measures in the context of a randomized-controlled trial of a research-based intervention integrated into Head Start programs (Head Start REDI). Three hundred fifty-six 4-year-old children (17% Hispanic, 25% African American; 54% girls) were followed over the course of the prekindergarten year. Initial EF predicted gains in cognitive and social–emotional skills and moderated the impact of the Head Start REDI intervention on some outcomes. The REDI intervention promoted gains on two EF measures, which partially mediated intervention effects on school readiness. We discuss the importance of further study of the neurobiological bases of school readiness, the implications for intervention design, and the value of incorporating markers of neurobiological processes into school readiness interventions.

Animal studies reveal that early deprivation impairs regulation of the hypothalamic–pituitary–adrenocortical (HPA) axis, potentially increasing vulnerability to stressors throughout life. To examine early deprivation effects on basal HPA axis activity in humans, basal cortisol levels were examined in 164 internationally adopted children who had experienced varying degrees of preadoption deprivation. Duration of institutional care, age at adoption, and parent ratings of preadoption neglect indexed a latent factor of Deprived Care. Adoption measures of height and weight standardized to World Health Organisation norms indexed a latent factor of Growth Delay that was viewed as another reflection of deprivation. Cortisol samples were collected 3.3–11.6 years postadoption (Md = 7.3 years) at home on 3 days approximately 30 min after wakeup and before bedtime. Both early a.m. levels and the decrease in cortisol across the day were examined. A structural equation model revealed that preadoption Deprived Care predicted Growth Delay at adoption and Growth Delay predicted higher morning cortisol levels and a larger diurnal cortisol decrease.

Autism is a neurodevelopmental disorder characterized by social and communication deficits, and repetitive behavior. Studies investigating the integrity of brain systems in autism suggest a wide range of gray and white matter abnormalities that are present early in life and change with development. These abnormalities predominantly affect association areas and undermine functional integration. Executive function, which has a protracted development into adolescence and reflects the integration of complex widely distributed brain function, is also affected in autism. Evidence from studies probing response inhibition and working memory indicate impairments in these core components of executive function, as well as compensatory mechanisms that permit normative function in autism. Studies also demonstrate age-related improvements in executive function from childhood to adolescence in autism, indicating the presence of plasticity and suggesting a prolonged window for effective treatment. Despite developmental gains, mature executive functioning is limited in autism, reflecting abnormalities in wide-spread brain networks that may lead to impaired processing of complex information across all domains.