Evidence regarding the use of inner speech by individuals with autism spectrum disorder (ASD) is equivocal. To clarify this issue, the current study employed multiple techniques and tasks used across several previous studies. In Experiment 1, participants with and without ASD showed highly similar patterns and levels of serial recall for visually presented stimuli. Both groups were significantly affected by the phonological similarity of items to be recalled, indicating that visual material was spontaneously recoded into a verbal form. Confirming that short-term memory is typically verbally mediated among the majority of people with ASD, recall performance among both groups declined substantially when inner speech use was prevented by the imposition of articulatory suppression during the presentation of stimuli. In Experiment 2, planning performance on a tower of London task was substantially detrimentally affected by articulatory suppression among comparison participants, but not among participants with ASD. This suggests that planning is not verbally mediated in ASD. It is important that the extent to which articulatory suppression affected planning among participants with ASD was uniquely associated with the degree of their observed and self-reported communication impairments. This confirms a link between interpersonal communication with others and intrapersonal communication with self as a means of higher order problem solving.

This study examined physiological correlates (cortisol and α-amylase [AA]) of peer victimization and aggression in a sample of 228 adolescents (45% male, 55% female; 90% African American; M age = 14 years, SD = 1.6 years) who participated in a longitudinal study of stress, physiology, and adjustment. Adolescents were classified into victimization/aggression groups based on patterns with three waves of data. At Wave 3, youth completed the Social Competence Interview (SCI), and four saliva samples were collected prior to, during, and following the SCI. Repeated-measures analyses of variance with victimization/aggression group as the predictor, and physiological measures as outcomes, controlling for time of day, pubertal status, and medication use revealed significant Group × SCI Phase interactions for salivary AA (sAA), but not for cortisol. The results did not differ by sex. For analyses with physical victimization/aggression, aggressive and nonaggressive victims showed increases in sAA during the SCI, nonvictimized aggressors showed a decrease, and the normative contrast group did not show any change. For analyses with relational victimization/aggression, nonaggressive victims were the only group who demonstrated sAA reactivity. Incorporating physiological measures into peer victimization studies may give researchers and clinicians insight into youth's behavior regulation, and help shape prevention or intervention efforts.

The study of gene expression (i.e., the study of the transcriptome) in different cells and tissues allows us to understand the molecular mechanisms of their differentiation, development and functioning. In this article, we describe some studies of gene-expression profiling for the purposes of understanding developmental (age-related) changes in the brain using different technologies (e.g., DNA-Microarray) and the new and increasingly popular RNA-Seq. We focus on advancements in studies of gene expression in the human brain, which have provided data on the structure and age-related variability of the transcriptome in the brain. We present data on RNA-Seq of the transcriptome in three distinct areas of the neocortex from different ages: mature and elderly individuals. We report that most age-related transcriptional changes affect cellular signaling systems, and, as a result, the transmission of nerve impulses. In general, the results demonstrate the high potential of RNA-Seq for the study of distinctive features of gene expression among cortical areas and the changes in expression through normal and atypical development of the central nervous system.

Past studies have shown that aggressive children exhibit rigid (rather than flexible) parent–child interactions; these rigid repertoires may provide the context through which children fail to acquire emotion-regulation skills. Difficulties in regulating emotion are associated with minimal activity in dorsal systems in the cerebral cortex, for example, the anterior cingulate cortex. The current study aimed to integrate parent–child and neurocognitive indices of emotion regulation and examine their associations for the first time. Sixty children (8–12 years old) referred for treatment for aggression underwent two assessments. Brain processes related to emotion regulation were assessed using dense-array EEG with a computerized go/no-go task. The N2 amplitudes thought to tap inhibitory control were recorded, and a source analysis was conducted. In the second assessment, parents and children were videotaped while trying to solve a conflict topic. State space grids were used to derive two dynamic flexibility parameters from the coded videotapes: (a) the number of transitions between emotional states and (b) the dispersion of emotional states, based on proportional durations in each state. The regression results showed that flexibility measures were not related to N2 amplitudes. However, flexibility measures were significantly associated with the ratio of dorsal to ventral source activation: for transitions, ΔR2 = .27, F (1, 34) = 13.13, p = .001; for dispersion, ΔR2 = .29, F (1, 35) = 14.76, p < .001. Thus, in support of our main hypothesis, greater dyadic flexibility was associated with a higher ratio of dorsomedial to ventral activation, suggesting that children with more flexible parent–child interactions are able to recruit relatively more dorsomedial activity in challenging situations.

This article represents an effort to extend our understanding of paranoia or suspicion and its development by integrating findings across clinical, developmental, and neuroscience literatures. We first define “paranoia” or paranoid thought and examine its prevalence across typically and atypically developing individuals and theoretical perspectives regarding its development and maintenance. We then briefly summarize current ideas regarding the neural correlates of adaptive, appropriately trusting interpersonal perception, social cognition, and behavior across development. Our focus shifts subsequently to examining in normative and atypical developmental contexts the neural correlates of several component cognitive processes thought to contribute to paranoid thinking: (a) attention bias for threat, (b) jumping to conclusions biases, and (c) hostile intent attribution biases. Where possible, we also present data regarding independent links between these cognitive processes and aggressive behavior. By examining data regarding the behavioral and neural correlates of varied cognitive processes that are likely components of a paranoid thinking style, we hope to advance both theoretical and empirical research in this domain.

Private speech (PS) and inner speech (IS) are thought to be functionally important for children's and adults’ cognition, but they have not been studied systematically in children with specific language impairment (SLI). Participants were 21 children with SLI (7–11 years, expressive or receptive verbal IQ ≤ 75, nonverbal IQ ≥ 84) and 21 age- and nonverbal IQ-matched controls. Participants completed three sets of Tower of London problems: one with no dual task (PS condition), one with articulatory suppression, and one while foot tapping (control condition). Participants also completed a digit span task. There was no group difference in the susceptibility of Tower of London performance to articulatory suppression, but the PS of the SLI group was less internalized than that of the controls on both tasks. The findings suggest that children with SLI experience a significant delay in the development of PS/IS, but that their PS/IS is effective for Tower of London performance in middle childhood. Findings are discussed with reference to the interpretation of the nonlinguistic deficits associated with SLI, and in terms of clinical implications.

The recent introduction of the induced pluripotent stem cell technology has made possible the derivation of neuronal cells from somatic cells obtained from human individuals. This in turn has opened new areas of investigation that can potentially bridge the gap between neuroscience and psychopathology. For the first time we can study the cell biology and genetics of neurons derived from any individual. Furthermore, by recapitulating in vitro the developmental steps whereby stem cells give rise to neuronal cells, we can now hope to understand factors that control typical and atypical development. We can begin to explore how human genes and their variants are transcribed into messenger RNAs within developing neurons and how these gene transcripts control the biology of developing cells. Thus, human-induced pluripotent stem cells have the potential to uncover not only what aspects of development are uniquely human but also variations in the series of events necessary for normal human brain development that predispose to psychopathology.

Cardiovascular response patterns to laboratory-based social and physical exercise challenges were evaluated in 69 children and adolescents, 20 with selective mutism (SM), to identify possible neurophysiological mechanisms that may mediate the behavioral features of SM. Results suggest that SM is associated with a dampened response of the vagal brake to physical exercise that is manifested as reduced reactivity in heart rate and respiration. Polyvagal theory proposes that the regulation of the vagal brake is a neurophysiological component of an integrated social engagement system that includes the neural regulation of the laryngeal and pharyngeal muscles. Within this theoretical framework, sluggish vagal brake reactivity may parallel an inability to recruit efficiently the structures involved in speech. Thus, the findings suggest that dampened autonomic reactivity during mobilization behaviors may be a biomarker of SM that can be assessed independent of the social stimuli that elicit mutism.

Children of depressed parents are significantly more likely to develop depression and other mental health disorders than are children of never-depressed parents. Investigations of the physiological mechanisms underlying this elevated risk have generally focused on basal functioning. It is important to note, however, that physiological reactivity or responses to stress are also critical determinants of mental and physical health. In the current study, we examined whether children of depressed parents exhibit altered physiological responses to stress. In two studies, never-depressed adolescent daughters of either recurrently depressed mothers (RISK) or never-depressed mothers (CTL) underwent social stressors while their physiological responses were measured (cortisol in Study 1, heart rate in Study 2). In both studies, affective responses to the stressors predicted physiological responses in RISK girls, but not in never-depressed girls. For RISK girls, decreased positive affect in response to stress predicted increased cortisol reactivity; in addition, decreased positive affect and increased negative affect were associated with poorer heart rate recovery and habituation, respectively. Future research is needed to examine explicitly whether this coherence between affect and physiology is a mechanism underlying the increased risk for psychopathology in children of depressed parents.

It has been reported that borderline personality related characteristics can be observed in children, and that these characteristics are associated with increased risk for the development of borderline personality disorder. It is not clear whether borderline personality related characteristics in children share etiological features with adult borderline personality disorder. We investigated the etiology of borderline personality related characteristics in a longitudinal cohort study of 1,116 pairs of same-sex twins followed from birth through age 12 years. Borderline personality related characteristics measured at age 12 years were highly heritable, were more common in children who had exhibited poor cognitive function, impulsivity, and more behavioral and emotional problems at age 5 years, and co-occurred with symptoms of conduct disorder, depression, anxiety, and psychosis. Exposure to harsh treatment in the family environment through age 10 years predicted borderline personality related characteristics at age 12 years. This association showed evidence of environmental mediation and was stronger among children with a family history of psychiatric illness, consistent with diathesis–stress models of borderline etiology. Results indicate that borderline personality related characteristics in children share etiological features with borderline personality disorder in adults and suggest that inherited and environmental risk factors make independent and interactive contributions to borderline etiology.

We propose that neuroscientific understanding of antisocial behavior can be advanced by focusing programmatic efforts on neurobehavioral trait constructs, that is, individual difference constructs with direct referents in neurobiology as well as behavior. As specific examples, we highlight inhibitory control and defensive reactivity as two such constructs with clear relevance for understanding antisocial behavior in the context of development. Variations in inhibitory control are theorized to reflect individual differences in the functioning of brain systems that operate to guide and inhibit behavior and regulate emotional response in the service of nonimmediate goals. Variations in defensive reactivity are posited to reflect individual differences in the sensitivity of the brain's aversive motivational (fear) system. We describe how these constructs have been conceptualized in the adult and child literatures and review work pertaining to traditional psychometric (rating and behaviorally based) assessment of these constructs and their known physiological correlates at differing ages as well as evidence linking these constructs to antisocial behavior problems in children and adults. We outline a psychoneurometric approach, which entails systematic development of neurobiological measures of target trait constructs through reference to psychological phenotypes, as a paradigm for linking clinical disorders to neurobiological systems. We provide a concrete illustration of this approach in the domain of externalizing proneness and discuss its broader implications for research on conduct disorder, antisocial personality, and psychopathy.

Improvements in temperance, perspective, and responsibility are a part of typical development of psychosocial maturity during adolescence. The existing literature suggests that the developmental course of psychosocial maturity is influenced by normative variations in social context, but little is known about how atypical contexts, such as incarceration, influence its development. The study investigates how the development of psychosocial maturity is affected by incarceration, using data from a 7-year longitudinal study of 1,171 adolescent males. We compared the effects of confinement in juvenile facilities with varying degrees of focus on incarceration versus rehabilitation (i.e., secure vs. residential treatment facilities) and tested whether facility quality and age at incarceration moderate the effect of incarceration on psychosocial maturity. The results indicate that incarceration in a secure setting, but not a residential treatment facility, is associated with a short-term decline in temperance and responsibility. The total amount of time incarcerated in a residential treatment facility, but not a secure setting, had a negative effect on the developmental trajectory of psychosocial maturity. Age at incarceration, but not the facility quality, moderated the effect of recent incarceration: older youths were more susceptible to short-term negative effects of recent incarceration in a secure setting, but they also benefited more than younger participants from short-term positive effects of incarceration in a residential treatment setting. Furthermore, youths who perceived their incarceration setting as unsafe evinced a decline in temperance. Future research and policy implications are discussed.

The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course.

Social support and vagal regulatory capacity (VRC), an index of flexible vagal responses during various types of stress, are linked to attenuated stress responding and positive health outcomes. Guided by the polyvagal perspective, we tested whether children's VRC is associated with attenuated sympathetic nervous system (SNS) stress reactivity in socially supportive conditions. Sixty-one 4- to 5-year-old children living in poverty underwent two standardized laboratory stress induction procedures. Cardiac vagal reactivity (respiratory sinus arrhythmia) to a first set of stressors (social, cognitive, physical, and emotional) indexed VRC. During a second set of stressors, participants were randomly assigned to a supportive or nonsupportive social context, and cardiac sympathetic reactivity (preejection period) was assessed. We hypothesized VRC would predict lower SNS stress reactivity, but only in the socially supportive context. Children with high VRC showed attenuated SNS stress reactivity in the socially supportive context compared to children with high VRC in the nonsupportive context and children with low VRC in either context. Individual differences in VRC predict attenuated SNS stress reactivity in socially supportive conditions. Understanding how social support and VRC jointly mitigate SNS stress reactivity may further efforts to prevent negative health outcomes. Implications for biological sensitivity to context and differential susceptibility theories are discussed.

The longitudinal associations of older sibling substance use as well as dyadic sibling conflict and collusion to younger sibling substance use were examined in a community-based sample of 244 same-sex sibling pairs. Indirect effects of older siblings on younger sibling substance use were hypothesized via younger sibling deviant peer affiliation and conflict with friends. Adolescents, parents, friends, and teachers completed measures of substance use, conflict, and deviant peer involvement. Observational data were used for both measures of collusion and conflict. Findings suggest that older sibling substance use has a direct effect on younger sibling use, but relationship dynamics and reinforcement played a significant role as well. Specifically, collusion and conflict in the sibling relationship both had indirect effects through younger siblings’ deviant peer affiliation. Findings validate the powerful socializing role of both siblings and peers, and elucidate the complex mechanisms through which socialization occurs. Furthermore, data underscore the importance of considering how multiple dimensions of socialization operate in the elaboration of antisocial behavior.

This research investigated whether exposure to peer stress serves as one pathway through which pubertal development contributes to depression over time, differentially for girls and boys. Youth (N = 149; 9.6–14.8 years) and their caregivers provided information at two waves, 1 year apart, on puberty (Wave 1), peer stress (occurring between Waves 1 and 2), and depression (Waves 1 and 2). Structural equation modeling analyses examined sex differences in the extent to which peer stress mediated the impact of pubertal status and timing on subsequent depression (i.e., tests of moderated mediation). Significant sex-moderated mediation was found for both pubertal status and timing. As indicated by moderate effect proportions, in girls, heightened peer stress partially mediated the longitudinal association between (a) more advanced pubertal status and depression; and (b) linear, but not curvilinear, pubertal timing (i.e., earlier maturation) and depression. This research contributes to our growing understanding of the interplay among physical, psychological, and social processes involved in the sex difference in adolescent depression.

Accumulating research suggests that psychopathy can be disaggregated into low-anxious primary and high-anxious secondary variants, and this research may be important for understanding antisocial youths with callous–unemotional traits. Using model-based cluster analysis, the present study disaggregated 165 serious male adolescent offenders (M age = 16) with high scores on the Youth Psychopathic Traits Inventory into primary and secondary variants based on the presence of anxiety. The results indicated that the secondary, high-anxious variant was more likely to show a history of abuse and scored higher on measures of emotional and attentional problems. On a picture version of the dot-probe task, the low-anxious primary variant was not engaged by emotionally distressing pictures, whereas the high-anxious secondary variant was more attentive to such stimuli (Cohen d = 0.71). Although the two groups differed as hypothesized from one another, neither differed significantly in their emotional processing from a nonpsychopathic control group of offending youth (n = 208). These results are consistent with the possibility that the two variants of psychopathy, both of which were high on callous–unemotional traits, may have different etiological pathways, with the primary being more related to a deficit in the processing of distress cues in others and the secondary being more related to histories of abuse and emotional problems.

Using behavioral and blood oxygen level dependent (BOLD) response indices through functional magnetic resonance imaging (fMRI), the current study investigated whether youths with disruptive behavior disorders (conduct disorder and oppositional defiant disorder) plus psychopathic traits (DBD + PT) show aberrant sensitivity to eye gaze information generally and/or whether they show particular insensitivity to eye gaze information in the context of fearful expressions. The participants were 36 children and adolescents (ages 10–17 years); 17 had DBD + PT and 19 were healthy comparison subjects. Participants performed a spatial attention paradigm where spatial attention was cued by eye gaze in faces displaying fearful, angry, or neutral affect. Eye gaze sensitivity was indexed both behaviorally and as BOLD response. There were no group differences in behavioral response: both groups showed significantly faster responses if the target was in the congruent spatial direction indicated by eye gaze. Neither group showed a Congruence × Emotion interaction; neither group showed an advantage from the displayer's emotional expression behaviorally. However, the BOLD response revealed a significant Group × Congruence × Emotion interaction. The comparison youth showed increased activity within the dorsal endogenous orienting network (superior parietal lobule and inferior parietal sulcus) for fearful congruent relative to incongruent trials relative to the youth with DBD + PT. The results are discussed with reference to current models of DBD + PT and possible treatment innovations.