Adolescence is a period marked by increases in risk taking, sensation seeking, and emotion dysregulation. Neurobiological models of adolescent development propose that lagging development in brain regions associated with affect and behavior control compared to regions associated with reward and emotion processing may underlie these behavioral manifestations. Cross-sectional studies have identified several functional brain networks that may contribute to risk for substance use and psychopathology in adolescents. Determining brain structure measures that prospectively predict substance use and psychopathology could refine our understanding of the mechanisms that contribute to these problems, and lead to improved prevention efforts. Participants (N = 265) were healthy substance-naïve adolescents (ages 12–14) who underwent magnetic resonance imaging and then were followed annually for up to 13 years. Cortical thickness and surface area measures for three prefrontal regions (dorsolateral prefrontal cortex, inferior frontal gyrus, and orbitofrontal cortex) and three cortical regions from identified functional networks (anterior cingulate cortex, insular cortex, and parietal cortex) were used to predict subsequent binge drinking, externalizing symptoms, and internalizing symptoms. Thinner dorsolateral prefrontal cortex and inferior frontal cortex in early adolescence predicted more binge drinking and externalizing symptoms, respectively, in late adolescence (ps < .05). Having a family history of alcohol use disorder predicted more subsequent binge drinking and externalizing symptoms. Thinner parietal cortex, but not family history, predicted more subsequent internalizing symptoms (p < .05). This study emphasizes the temporal association between maturation of the salience, inhibition, and executive control networks in early adolescence and late adolescent behavior outcomes. Our findings indicate that developmental variations in these brain regions predate behavioral outcomes of substance use and psychopathology, and may therefore serve as prospective biomarkers of vulnerability.

Early identification of problems with psychosocial stress regulation is important for supporting mental and physical health. However, we currently lack knowledge about when reliable individual differences in stress-responsive physiology emerge and which aspects of maternal behavior determine the unfolding of infants' stress responses. Knowledge of these processes is further limited by analytic approaches that do not account for multiple levels of within- and between-family effects. In a low-risk sample (n = 100 dyads), we observed infant cortisol and mother/infant behavior during regular play and stress sessions longitudinally from age 1 to 3, and used a three-level model to separately examine variability in infant cortisol trajectories within sessions, across years, and across infants. Stable individual differences in hypothalamus–pituitary–adrenal axis regulation were observed in the first 3 years of life. Infants of less sensitive and more intrusive mothers manifested stress sensitization, that is, elevated cortisol levels during and following stress exposure, a profile related to behavioral distress. These findings have important practical implications, suggesting that children at risk for long-term stress dysregulation may be identified in the earliest years of life.

Much research has examined Moffitt's developmental taxonomy, focusing almost exclusively on the distinction between life-course persistent and adolescence-limited offenders. Of interest, a handful of studies have identified a group of individuals whose early childhood years were marked by extensive antisocial behavior but who seemed to recover and desist (at least from severe offending) in adolescence and early adulthood. We use data from the Cambridge Study in Delinquent Development to examine the adult adjustment outcomes of different groups of offenders, including a recoveries group, in late middle adulthood, offering the most comprehensive investigation of this particular group to date. Findings indicate that abstainers comprise the largest group of males followed by adolescence-limited offenders, recoveries, and life-course persistent offenders. Furthermore, the results reveal that a host of adult adjustment problems measured at ages 32 and 48 in a number of life-course domains are differentially distributed across these four offender groups. In addition, the recoveries and life-course persistent offenders often show the greatest number of adult adjustment problems relative to the adolescence-limited offenders and abstainers.

Internalizing symptoms during adolescence and beyond is a major public health concern, particularly because severe symptoms can lead to the diagnosis of a number of serious psychiatric conditions. This study utilizes a unique sample with a complex statistical method in order to explore Gene × Environment interactions found in internalizing symptoms during adolescence. Data for this study were drawn from a longitudinal prevention intervention study (n = 798) of Baltimore city school children. Internalizing symptom data were collected using self-report and blood or saliva samples genotyped using Affymetrix 6.0 microarrays. A major depression polygenic score was created for each individual using information from the major depressive disorder Psychiatric Genetics Consortium and used as a predictor in a latent trait–state–occasion model. The major depressive disorder polygenic score was a significant predictor of the stable latent trait variable, which captures time-independent phenotypic variability. In addition, an early childhood stressor of death or divorce was a significant predictor of occasion-specific variables. A Gene × Environment interaction was not a significant predictor of the latent trait or occasion variables. These findings support the importance of genetics on the stable latent trait portion of internalizing symptoms across adolescence.

A developmental cascade model from functioning in adolescence to emerging adulthood was tested using data from a 15-year longitudinal follow-up of 240 emerging adults whose families participated in a randomized, experimental trial of a preventive program for divorced families. Families participated in the program or literature control condition when the offspring were ages 9–12. Short-term follow-ups were conducted 3 months and 6 months following completion of the program when the offspring were in late childhood/early adolescence. Long-term follow-ups were conducted 6 years and 15 years after program completion when the offspring were in middle to late adolescence and emerging adulthood, respectively. It was hypothesized that the impact of the program on mental health and substance use outcomes in emerging adulthood would be explained by developmental cascade effects of program effects in adolescence. The results provided support for a cascade effects model. Specifically, academic competence in adolescence had cross-domain effects on internalizing problems and externalizing problems in emerging adulthood. In addition, adaptive coping in adolescence was significantly, negatively related to binge drinking. It was unexpected that internalizing symptoms in adolescence were significantly negatively related to marijuana use and alcohol use. Gender differences occurred in the links between mental health problems and substance use in adolescence and mental health problems and substance use in emerging adulthood.

Previous studies have documented the serotonin transporter linked polymorphic region (5-HTTLPR) as a genetic susceptibility variant that contributes to variability in outcomes related to affective psychopathology, with the short allele associated with negative affectivity and the long allele associated with positive affectivity. In a separate but related line of research, extensive evidence suggests that frontal electroencephalography (EEG) hemispheric asymmetry in the alpha band is also associated with risk for affective psychopathologies, with leftward asymmetry associated with approach-related behavior patterns and rightward frontal EEG asymmetry associated with withdrawn behavioral tendencies. We examined frontal EEG hemispheric asymmetries in relation to 5-HTTLPR genotyping in 70 children between 4 and 6 years of age. Analyses revealed that frontal EEG lateralization interacted with genotype such that children homozygous for the short allele exhibited rightward frontal EEG asymmetries, children who were homozygous for the long allele consistently exhibited a positive pattern of leftward asymmetry, and heterozygotes exhibited equivalent left and right frontal activity. These findings suggest that the 5-HTTLPR short allele may provide a degree of susceptibility for later affective psychopathology in adolescence and adulthood, through mediation of frontal brain activity that is associated with cognitive–behavioral withdrawal tendencies and negative affectivity.

Many young adolescents are embedded in neighborhoods, schools, and homes where alcohol and drugs are frequently used. However, little is known about (a) how witnessing others' substance use affects adolescents in their daily lives and (b) which adolescents will be most affected. The current study used ecological momentary assessment with 151 young adolescents (ages 11–15) to examine the daily association between witnessing substance use and antisocial behavior across 38 consecutive days. Results from multilevel logistic regression models indicated that adolescents were more likely to engage in antisocial behavior on days when they witnessed others using substances, an association that held when substance use was witnessed inside the home as well as outside the home (e.g., at school or in their neighborhoods). A significant Gene × Environment interaction suggested that the same-day association between witnessing substance use and antisocial behavior was significantly stronger among adolescents with, versus without, the dopamine receptor D4 seven repeat (DRD4-7R) allele. The implications of the findings for theory and research related to adolescent antisocial behavior are discussed.

Childhood maltreatment can disturb brain development and subsequently lead to adverse socioemotional and mental health problems across the life span. The long-term association between childhood maltreatment and resting–wake brain activity during adulthood is unknown and was examined in the current study. Forty-one medically stable and medication-free military veterans (M = 29.31 ± 6.01 years, 78% male) completed a battery of clinical assessments and had [18F]-fluorodeoxyglucose positron emission tomography neuroimaging scans during quiet wakefulness. After statistically adjusting for later-life trauma and mental health problems, childhood maltreatment was negatively associated with brain activity within a priori defined regions that included the left orbital frontal cortex and left hippocampus. Childhood maltreatment was significantly associated with increased and decreased brain activity within six additional whole-brain clusters that included the frontal, parietal–temporal, cerebellar, limbic, and midbrain regions. Childhood maltreatment is associated with altered neural activity in adulthood within regions that are involved in executive functioning and cognitive control, socioemotional processes, autonomic functions, and sleep/wake regulation. This study provides support for taking a life span developmental approach to understanding the effects of early-life maltreatment on later-life neurobiology, socioemotional functioning, and mental health.

Few studies have investigated developmental strengths and weaknesses within the cognitive profile of children and adolescents with fragile X syndrome (FXS), a single-gene cause of inherited intellectual impairment. With a prospective longitudinal design and using normalized raw scores (Z scores) to circumvent floor effects, we measured cognitive functioning of 184 children and adolescents with FXS (ages 6 to 16) using the Wechsler Scale of Intelligence for Children on one to three occasions for each participant. Participants with FXS received lower raw scores relative to the Wechsler Scale of Intelligence for Children normative sample across the developmental period. Verbal comprehension, perceptual organization, and processing speed Z scores were marked by a widening gap from the normative sample, while freedom from distractibility Z scores showed a narrowing gap. Key findings include a relative strength for verbal skills in comparison with visuospatial–constructive skills arising in adolescence and a discrepancy between working memory (weakness) and processing speed (strength) in childhood that diminishes in adolescence. Results suggest that the cognitive profile associated with FXS develops dynamically from childhood to adolescence. Findings are discussed within the context of aberrant brain morphology in childhood and maturation in adolescence. We argue that assessing disorder-specific cognitive developmental profiles will benefit future disorder-specific treatment research.

A total of 149 children, who spent an average of 13.8 months in Russian institutions, were transferred to Russian families of relatives and nonrelatives at an average age of 24.7 months. After residing in these families for at least 1 year (average = 43.2 months), parents reported on their attachment, indiscriminately friendly behavior, social–emotional competencies, problem behaviors, and effortful control when they were 1.5–10.7 years of age. They were compared to a sample of 83 Russian parents of noninstitutionalized children, whom they had reared from birth. Generally, institutionalized children were rated similarly to parent-reared children on most measures, consistent with substantial catch-up growth typically displayed by children after transitioning to families. However, institutionalized children were rated more poorly than parent-reared children on certain competencies in early childhood and some attentional skills. There were relatively few systematic differences associated with age at family placement or whether the families were relatives or nonrelatives. Russian parent-reared children were rated as having more problem behaviors than the US standardization sample, which raises cautions about using standards cross-culturally.

Individuals with autism spectrum disorder (ASD) experience higher rates of psychopathology than their typically developing peers or peers with other intellectual or developmental disabilities. Little is known about the developmental course of psychiatric symptoms such as internalizing and externalizing behaviors in this population. Individual characteristics and aspects of the family environment may explain variability in outcomes for adults with ASD. The present study extends our current understanding of psychopathology among individuals with ASD by examining group-based trajectories of internalizing and externalizing symptoms in adulthood. Overall, the results showed that symptoms became less severe over time. Distinct patterns of change in psychopathology were observed and associated with differential profiles of psychotropic medication use, comorbid mental health diagnoses, and residential placement. The likelihood of following each developmental trajectory was estimated based on characteristics of the adults with ASD (gender, adaptive behavior, and autistic symptoms) and maternal expressed emotion (criticism and warmth). Maternal criticism and warmth were identified as key risk and protective factors, respectively, with important implications for future research and intervention for individuals with ASD.

Temperament and parental practices (PP) are important predictors of adolescent alcohol use (AU); however, less is known about how they combine to increase or decrease risk of AU. This study examined whether age 6 temperament (i.e., impulsivity and inhibitory control) interacted with age 6 coercive PP and/or age 14 parental monitoring to predict AU at 15 years among 209 adolescents. Results showed that low parental monitoring was associated with more frequent AU and that coercive PP interacted with impulsivity to predict AU. This interaction was examined as a function of two models that were not studied before in the prediction of AU: the diathesis–stress model (i.e., impulsive children are more “vulnerable” to adverse PP than those with an easy temperament); and the differential susceptibility model (i.e., impulsive children are also more likely to benefit from good PP). Results supported the differential susceptibility model by showing that impulsive children were not only at higher risk for AU when combined with high coercive PP but also benefit from the absence of coercive PP. This supports the suggestion that the conception of certain temperament characteristics, or in this case impulsivity, as a “vulnerability” for adolescent AU, may need revision because it misrepresents the malleability it may imply.

Several studies suggest that neighborhood deprivation is a unique risk factor in child and adolescent development of problem behavior. We sought to examine whether previously established intervention effects of the Family Check-Up (FCU) on child conduct problems at age 7.5 would persist through age 9.5, and whether neighborhood deprivation would moderate these effects. In addition, we examined whether improvements in parent–child interaction during early childhood associated with the FCU would be related to later reductions in child aggression among families living in the highest risk neighborhoods. Using a multisite cohort of at-risk children identified on the basis of family, child, and socioeconomic risk and randomly assigned to the FCU, intervention effects were found to be moderated by neighborhood deprivation, such that they were only directly present for those living at moderate versus extreme levels of neighborhood deprivation. In addition, improvements in child aggression were evident for children living in extreme neighborhood deprivation when parents improved the quality of their parent–child interaction during the toddler period (i.e., moderated mediation). Implications of the findings are discussed in relation to the possibilities and possible limitations in prevention of early problem behavior for those children living in extreme and moderate levels of poverty.

Drawing from developmental psychology and psychopathology, we propose a new, developmentally informed approach to parenting interventions that focuses on elucidating changes in the unfolding developmental process between the parent and child. We present data from 186 low-income mothers of toddlers, randomly assigned to a child-oriented play group or a play-as-usual group. We examined the maladaptive cascade from child difficulty to mother adversarial, negative parenting to child maladjustment, well documented in the literature. The measures incorporated multiple observations and reports. As expected, the sequence from child difficulty (pretest) to mother adversarial, negative parenting (Posttest 1, after 3-month intervention) to child maladjustment (Posttest 2, 6 months later) was present in the play-as-usual group, but absent, or defused, in the child-oriented play group. The findings are consistent with a view of intervention presumably enhancing the mother–child relationship, which in turn served to moderate future mother–child dynamics, altering its otherwise anticipated negative trajectory. A closer examination of the cascade revealed that, at Posttest 1, mothers in the play-as-usual group engaged in more adversarial, negative parenting (controlling for pretest) than did mothers in the child-oriented play group when their children were of high difficulty. The intervention appears to exert its primary influence on the cascade by weakening the link between child difficulty and maternal adversarial, negative parenting.

Rates of self-inflicted injury among adolescents have risen in recent years, yet much remains to be learned about the pathophysiology of such conduct. Self-injuring adolescents report high levels of both impulsivity and depression behaviorally. Aberrant neural responding to incentives, particularly in striatal and prefrontal regions, is observed among both impulsive and depressed adolescents, and may mark common vulnerability to symptoms of anhedonia, irritability, and low positive affectivity. To date, however, no studies have examined associations between central nervous system reward responding and self-injury. In the current study, self-injuring (n = 19) and control (n = 19) adolescent females, ages 13–19 years, participated in a monetary incentive delay task in which rewards were obtained on some trials and losses were incurred on others. Consistent with previous findings from impulsive and depressed samples, self-injuring adolescents exhibited less activation in both striatal and orbitofrontal cortex regions during anticipation of reward than did controls. Self-injuring adolescents also exhibited reduced bilateral amygdala activation during reward anticipation. Although few studies to date have examined amygdala activity during reward tasks, such findings are common among adults with mood disorders and borderline personality disorder. Implications for neural models of impulsivity, depression, heterotypic comorbidity, and development of both self-injury and borderline personality traits are discussed.