Search

Objective Most evidence for structural brain abnormalities associated with adolescent depression is based on cross-sectional study designs that do not take into account the dynamic course of depressive symptoms and brain maturation across adolescence. In this study, a longitudinal design was used to investigate the association between different trajectories of depressive symptoms and longitudinal changes in brain structure throughout adolescence. Method One hundred forty-nine adolescents were assessed on depressive symptoms and underwent structural magnetic resonance imaging at 12 years of age and were followed up multiple times until 19 years. Three depressive symptom trajectories (low-stable [n = 97], early-decreasing [n = 33], late-increasing [n = 19]) were identified, and effects of group and group by time on hippocampus and amygdala volume and prefrontal cortical thickness and surface area were evaluated. Results The early-decreasing symptoms group exhibited differences in cortical surface area compared to the low-stable and late-increasing symptoms groups, moderated by sex. Specifically, females in the early-decreasing symptoms group showed lower anterior cingulate and orbitofrontal cortex surface areas across adolescence compared to females in the other groups. Males in the early-decreasing symptoms group showed lower right orbitofrontal cortex surface area expansion over time compared to males in the low-stable and late-increasing symptoms groups. No effects were found for cortical thickness or for hippocampus and amygdala volume. Conclusion Alterations in cortical surface area were specifically observed in young people experiencing depressive symptoms in early adolescence. These findings suggest that early adolescence is a particularly sensitive period for cortical surface area abnormalities associated with depressive symptoms and could provide a critical window for treatment of (subthreshold) depressive symptoms.

OBJECTIVE: This study utilized a novel multisystem approach to investigate the effect of observed parental behavior on the relationship between biological mechanisms associated with disease processes (i.e., autonomic physiology and immune response) among their adolescent children. METHOD: Thirty-three adolescents (23 males), aged 11-13, and their parents participated in a laboratory session in which adolescents provided baseline measures of autonomic (sympathetic) activity, and adolescents and 1 parent participated in a laboratory based dyadic conflict resolution interaction task. This included 3 male parent/male adolescent dyads, 20 female parent/male adolescent dyads, 3 male parent/female adolescent dyads, and 7 female parent/female adolescent dyads. Approximately 3 years later, adolescents provided a salivary measure of C-Reactive Protein (sCRP) to index inflammation. RESULTS: Analyses revealed a positive association between sympathetic activity and sCRP, as well as a moderating role of positive parental behavior in this relationship, such that the association between sympathetic activity and sCRP was greater among adolescents whose parents displayed shorter duration of positive affect. CONCLUSIONS: Overall findings indicate parental behavior may influence the association between adolescent sympathetic activity and inflammatory processes. These findings have important implications for understanding the impact of psychosocial factors on biological mechanisms of disease. (PsycINFO Database Record

Background Extant research has demonstrated that parenting behaviour can be a significant contributor to the development of brain structure and mental health during adolescence. Nonetheless, there is limited research examining these relationships during late childhood, and particularly in the critical period of brain development occurring between 8 and 10 years of age. The effects of the family environment on the brain during late childhood may have significant implications for later functioning, and particularly mental health. The Families and Childhood Transitions Study (FACTS) is a multidisciplinary longitudinal cohort study of brain development and mental health, with two waves of data collection currently funded, occurring 18-months apart, when child participants are aged approximately 8- and 10-years old. Methods/design Participants are 163 children (M age [SD] = 8.44 [0.34] years, 76 males) and their mothers (M age [SD] = 40.34 [5.43] years). Of the 163 families who consented to participate, 156 completed a video-recorded and observer-coded dyadic interaction task and 153 completed a child magnetic resonance imaging brain scan at baseline. Families were recruited from lower socioeconomic status (SES) areas to maximise rates of social disadvantage and variation in parenting behaviours. All experimental measures and tasks completed at baseline are repeated at an 18-month follow-up, excluding the observer coded family interaction tasks. The baseline assessment was completed in October 2015, and the 18-month follow up will be completed May 2017. Discussion This study, by examining the neurobiological and mental health consequences of variations in parenting, has the potential to significantly advance our understanding of child development and risk processes. Recruitment of lower SES families will also allow assessment of resilience factors given the poorer outcomes often associated with this population. Electronic supplementary material The online version of this article (doi:10.1186/s12887-017-0905-x) contains supplementary material, which is available to authorized users.

Background Genes, molecules and neural circuits that are associated with, or confer risk to developing schizophrenia have been studied and mapped. It is hypothesized that certain neural systems may counterbalance familial risk of schizophrenia, and thus confer resilience to developing the disorder. This study sought to identify resting-state functional brain connectivity (rs-FC) representing putative risk or resilience endophenotypes in schizophrenia. Methods Resting-state functional magnetic resonance imaging (rs-fMRI) was performed in 42 individuals with treatment resistant schizophrenia (TRS), 16 unaffected first-degree family members (UFM) and 42 healthy controls. Whole-brain rs-FC networks were mapped for each individual and analysed graph theoretically to identify network markers associated with schizophrenia risk or resilience. Results The ~ 900 functional connections showing between-group differences were operationalized as conferring: i) resilience, ii) risk, or iii) precipitating risk and/or illness effects. Approximately 95% of connections belonged to the latter two categories, with substantially fewer connections associated with resilience. Schizophrenia risk primarily involved reduced frontal and occipital rs-FC, with patients showing additional reduced frontal and temporal rs-FC. Functional brain networks were characterized by greater local efficiency in UFM, compared to TRS and controls. Conclusions TRS and UFM share frontal and occipital rs-FC deficits, representing a ‘risk’ endophenotype. Additional reductions in frontal and temporal rs-FC appear to be associated with risk that precipitates psychosis in vulnerable individuals, or may be due to other illness-related effects, such as medication. Functional brain networks are more topologically resilient in UFM compared to TRS, which may protect UFM from psychosis onset despite familial liability.

Changes in the functional connectivity of the subgenual anterior cingulate cortex (SGC) have been linked with depressive symptoms. The aim of this study was to map this relationship across mid to late adolescence. Employing a longitudinal functional magnetic resonance imaging (fMRI) design, associations between patterns of resting-state SGC functional connectivity and symptoms of depression were examined at two time points in an initial sample of 72 adolescents. Using a region-of-interest approach, these associations were evaluated cross-sectionally and longitudinally. Cross-sectionally, weaker SGC functional connectivity with the posterior cingulate cortex (PCC), angular gyrus and dorsal prefrontal cortex at baseline, and weaker SGC connectivity with the dorsomedial prefrontal cortex (DMPFC) and ventromedial prefrontal cortex at follow-up, were associated with higher depressive symptoms. Longitudinally, a decrease in SGC functional connectivity with DMPFC, PCC, angular gyrus and middle temporal gyrus was associated with higher depressive symptoms at follow-up. The observation of weaker SGC connectivity predicting increased symptoms contrasts with the majority of resting-state fMRI studies in clinically depressed populations. Taken together with these past studies, our findings suggest depression-related changes in SGC functional connectivity may differ across developmental and illness stages.

Background Altered basal ganglia function has been implicated in the pathophysiology of youth Major Depressive Disorder (MDD). Studies have generally focused on characterizing abnormalities in ventral “affective” corticostriatal loops supporting emotional processes. Recent evidence however, has implicated alterations in functional connectivity of dorsal “cognitive” corticostriatal loops in youth MDD. The contribution of dorsal versus ventral corticostriatal alterations to the pathophysiology of youth MDD remains unclear. Methods Twenty-one medication-free patients with moderate-to-severe MDD between the ages of 15 and 24 years old were matched with 21 healthy control participants. Using resting-state functional connectivity magnetic resonance imaging we systematically investigated connectivity of eight dorsal and ventral subdivisions of the striatum. Voxelwise statistical maps of each subregion's connectivity with other brain areas were compared between the depressed and control groups. Results Depressed youths showed alterations in functional connectivity that were confined to the dorsal corticostriatal circuit. Compared to controls, depressed patients showed increased connectivity between the dorsal caudate nucleus and ventrolateral prefrontal cortex bilaterally. Increased depression severity correlated with the magnitude of dorsal caudate connectivity with the right dorsolateral prefrontal cortex. There were no significant between-group differences in connectivity of ventral striatal regions. Conclusions The results provide evidence that alterations in corticostriatal connectivity are evident at the early stages of the illness and are not a result of antidepressant treatment. Increased connectivity between the dorsal caudate, which is usually associated with cognitive processes, and the more affectively related ventrolateral prefrontal cortex may reflect a compensatory mechanism for dysfunctional cognitive-emotional processing in youth depression., Highlights • We systematically examine dorsal and ventral striatal connectivity in youth MDD. • Alterations in functional connectivity in youth MDD are confined to the dorsal circuit. • Youths with MDD show increased dorsal caudate connectivity with the VLPFC. • Altered dorsal caudate–VLPFC connectivity in MDD may reflect a compensatory response.

Trait positive affect (PA) in childhood confers both risk and resilience to psychological and behavioral difficulties in adolescence, although explanations for this association are lacking. Neurodevelopment in key areas associated with positive affect is ongoing throughout adolescence, and is likely to be related to the increased incidence of disorders of positive affect during this period of development. The aim of this study was to prospectively explore the relationship between trait indices of PA and brain development in subcortical reward regions during early to mid-adolescence in a community sample of adolescents. A total of 89 (46 male, 43 female) adolescents participated in magnetic resonance imaging assessments during both early and mid-adolescence (mean age at baseline = 12.6 years, SD = 0.45; mean follow-up period = 3.78 years, SD = 0.21) and also completed self-report measures of trait positive and negative affect (at baseline). To examine the specificity of these effects, the relation between negative affect and brain development was also examined. The degree of volume reduction in the right caudate over time was predicted by PA. Independent of time, larger hippocampal volumes were associated with higher PA, and negative affect was associated with smaller left amygdala volume. The moderating effect of negative affect on the development of the left caudate varied as a function of lifetime psychiatric history. These findings suggest that early to mid-adolescence is an important period whereby neurodevelopmental processes may underlie key phenotypes conferring both risk and resilience for emotional and behavioral difficulties later in life.

Highlights • Longitudinal study investigating the relationship between development of cortical thickness and effortful control during adolescence. • Examined whether change in effortful control mediated the relationship between cortical development and change in socioemotional functioning, including psychopathology symptoms. • Greater cortical thinning of the left ACC was associated with superior development of effortful control. • Changes in effortful control mediated the relationship between greater thinning of the left ACC and improvements in socioemotional functioning., This study investigated the relationship between the development of effortful control (EC), a temperamental measure of self-regulation, and concurrent development of three regions of the prefrontal cortex (anterior cingulate cortex, ACC; dorsolateral prefrontal cortex, dlPFC; ventrolateral prefrontal cortex, vlPFC) between early- and mid-adolescence. It also examined whether development of EC mediated the relationship between cortical maturation and emotional and behavioral symptoms. Ninety-two adolescents underwent baseline assessments when they were approximately 12 years old and follow-up assessments approximately 4 years later. At each assessment, participants had MRI scans and completed the Early Adolescent Temperament Questionnaire-Revised, as well as measures of depressive and anxious symptoms, and aggressive and risk taking behavior. Cortical thicknesses of the ACC, dlPFC and vlPFC, estimated using the FreeSurfer software, were found to decrease over time. EC also decreased over time in females. Greater thinning of the left ACC was associated with less reduction in EC. Furthermore, change in effortful control mediated the relationship between greater thinning of the left ACC and improvements in socioemotional functioning, including reductions in psychopathological symptoms. These findings highlight the dynamic association between EC and the maturation of the anterior cingulate cortex, and the importance of this relationship for socioemotional functioning during adolescence.

Investigating etiological processes early in the life span represents an important step toward a better understanding of the development of personality pathology. The current study evaluated the interaction between an individual difference risk factor (i.e., temperament) and a biological risk factor for aggressive behavior (i.e., atypical [larger] rightward hippocampal asymmetry) in predicting the emergence of borderline personality disorder (BPD) and antisocial personality disorder symptoms during early adolescence. The sample consisted of 153 healthy adolescents (M = 12.6 years, SD = 0.4, range = 11.4–13.7) who were selected from a larger sample to maximize variation in temperament. Interactions between four temperament factors (effortful control, negative affectivity, surgency, and affiliativeness), based on the Early Adolescent Temperament Questionnaire—Revised, and volumetric measures of hippocampal asymmetry were examined as cross-sectional predictors of BPD and antisocial personality disorder symptoms. Boys were more likely to have elevated BPD symptoms if they were high on affiliation and had larger rightward hippocampal asymmetry. In boys, low affiliation was a significant predictor of BPD symptoms in the presence of low rightward hippocampal asymmetry. For girls, low effortful control was associated with elevated BPD symptoms in the presence of atypical rightward hippocampal asymmetry. This study builds on previous work reporting significant associations between atypical hippocampal asymmetry and poor behavioral regulation.

Summary Objective To investigate the longitudinal relationship between pituitary gland volume (PGV) and parameters of hypothalamic-pituitary-adrenal axis (HPAA) functioning during adolescence. Methods Participants were 49 adolescents (19 girls and 30 boys) selected from a larger longitudinal, population-based study of adolescent development. Assessments were conducted at three time points (S1, S2 and S3). MRI sessions were at S1 (age: M = 12.62, SD = 0.45 years) and S3 (M = 16.48, SD = 0.53 years) and multiple assessments of salivary cortisol were undertaken at S2 (M = 15.51, SD = 0.35 years). PGV was measured via previously validated manual tracing methods, and the cortisol awakening response (CAR) and diurnal slope (DSL) were used as indices of HPAA functioning. Results A significant sex-linked interaction was found for PGV at S1 predicting both CAR (p = 0.025) and DSL (p = 0.009) at S2. Specifically, PGV at S1 significantly predicted CAR (p = 0.033) and DSL (p = 0.010) in boys only, with no significant results found for girls. Neither CAR nor DSL at S2 predicted growth of PGV from S1 to S3. Conclusions PGV in early adolescence predicted HPAA functioning in mid-adolescent boys but not in girls. The results suggest a significant influence of sex-specific development on the relationship between PGV and HPAA activity and reactivity. The findings have potential implications for understanding and interpreting sex-linked and stress related clinical disorders that emerge during mid-to-late adolescence.

In this study, we investigated the prospective relationship between maternal behaviors observed during mother-adolescent interactions and the onset of major depressive disorder (MDD) between early and late adolescence (ages 12–18). Maternal expressions of emotion and maternal responses to their child’s expressions of emotion were both examined. Results demonstrated that higher rates of maternal aggressive behavior and lower rates of maternal positive behavior prospectively predicted MDD onset across adolescence. In addition, negative (i.e., aggressive and dysphoric) maternal responses to adolescents’ aggressive and positive behaviors predicted MDD onset. Maternal dysphoric behavior and the way mothers respond to adolescents’ dysphoria were not related to MDD onset. These results extend previous findings on the relationship between parenting behaviors and depression onset in early to midadolescence and suggest that maternal emotion socialization behaviors in early adolescence prospectively predict MDD onset across the entire course of adolescence.

Early to mid-adolescence is an important developmental period for subcortical brain maturation, but longitudinal studies of these neurodevelopmental changes are lacking. The present study acquired repeated magnetic resonance images from 60 adolescent subjects (28 female) at ages 12.5 and 16.5 years to map changes in subcortical structure volumes. Automated segmentation techniques optimized for longitudinal measurement were used to delineate volumes of the caudate, putamen, nucleus accumbens, pallidum, hippocampus, thalamus and the whole brain. Amygdala volumes were described using manual tracing methods. The results revealed heterogeneous maturation across the regions of interest (ROIs), and change was differentially moderated by sex and hemisphere. The caudate, thalamus and putamen declined in volume, more for females relative to males, and decreases in the putamen and thalamus were greater in the left hemisphere. The pallidum increased in size, but more so in the left hemisphere. While the left nucleus accumbens increased in size, the right accumbens decreased in size over the follow-up period. Increases in hippocampal volume were greater in the right hemisphere. While amygdala volume did not change over time, the left hemisphere was consistently larger than the right. These results suggest that subcortical brain development from early to middle adolescence is characterized by striking hemispheric specialization and sexual dimorphisms, and provide a framework for interpreting normal and abnormal changes in cognition, affect and behavior. Moreover, the differences in findings compared to previous cross-sectional research emphasize the importance of within-subject assessment of brain development during adolescence.

The devastating social, emotional and economic consequences of human aggression are laid bare nightly on newscasts around the world. Aggression is principally mediated by neural circuitry comprising multiple areas of the prefrontal cortex and limbic system, including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), amygdala and hippocampus. A striking characteristic of these regions is their structural asymmetry about the midline (i.e. left vs right hemisphere). Variations in these asymmetries have been linked to clinical disorders characterized by aggression and the rate of aggressive behavior in psychiatric patients. Here, we show for the first time that structural asymmetries in prefrontal cortical areas are also linked to aggression in a normal population of early adolescents. Our findings indicate a relationship between parent reports of aggressive behavior in adolescents and structural asymmetries in the limbic and paralimbic ACC and OFC, and moreover, that this relationship varies by sex. Furthermore, while there was no relationship between aggression and structural asymmetries in the amygdala or hippocampus, hippocampal volumes did predict aggression in females. Taken together, the results suggest that structural asymmetries in the prefrontal cortex may influence human aggression, and that the anatomical basis of aggression varies substantially by sex.

Item does not contain fulltext Orbitofrontal cortex (OFC) sulcogyral patterns are stable morphological variations established early in life. They consist of three distinct pattern types, with Type III in particular being associated with poor regulatory control (e.g., high sensation seeking and negative emotionality, low constraint), which may confer risk for earlier onset of cannabis (CB) use and greater use in later life. The OFC sulcogyral pattern may therefore be a stable trait marker in understanding individual differences in substance-use vulnerability and associated affective disturbances in users. In a large multisite cross-sectional study, we compared OFC pattern type distribution between 128 healthy controls (HC) and 146 CB users. Within users (n=140), we explored the association between OFC pattern type and CB use level, and subsequently if level of CB use informed by OFC pattern type may mediate disturbances in affective tone, as indexed by depressive symptoms. While OFC pattern distribution did not distinguish between HC and CB groups, it informed greater lifetime use within users. Specifically, CB users with pattern Type III in the right OFC tended to use more CB over their lifetime, than did CB users with pattern Type I or II. Greater lifetime CB use was subsequently associated with higher depressive symptoms, such that it mediated an indirect association between right OFC pattern Type III and higher depressive symptoms. The present study provides evidence for neurobiological differences, specifically sulcogyral pattern of the OFC, to modulate level of CB use, which may subsequently influence the expression of depressive symptoms.

Introduction Up to 20% of individuals with schizophrenia show minimal or no response to medication and are considered to have ‘treatment-resistant’ schizophrenia (TRS). Unlike early and established schizophrenia, few studies have investigated resting-state functional connectivity (rs-FC) in TRS. Here, we test for disruptions in FC and altered efficiency of functional brain networks in a well-characterized cohort of TRS patients. Methods Resting-state functional magnetic resonance imaging was used to investigate functional brain networks in 42 TRS participants prescribed clozapine (30 males, mean age = 41.3(10)) and 42 healthy controls (24 males, mean age = 38.4(10)). Graph analysis was used to characterize between-group differences in local and global efficiency of functional brain network organization as well as the strength of FC. Results Global brain FC was reduced in TRS patients (p = 0.0001). Relative to controls, 3.4% of all functional connections showed reduced strength in TRS (p < 0.001), predominantly involving fronto-temporal, fronto-occipital and temporo-occipital connections. Global efficiency was reduced in TRS (p = 0.0015), whereas local efficiency was increased (p = 0.0042). Conclusions TRS is associated with widespread reductions in rs-FC and altered network topology. Increased local functional network efficiency coupled with decreased global efficiency suggests that hub-to-hub connections are preferentially affected in TRS. These findings further our understanding of the neurobiological impairments in TRS.

Gender differences in emotion experience and expression represent some of the most robust gender stereotypes worldwide. However, empirical support for these stereotypes is lacking, especially from research utilizing objective measures, such as neuroimaging methodologies. In this chapter, we review functional neuroimaging studies that have empirically tested for gender differences in the association between brain function and emotion processes (including perception, reactivity, regulation, and experience). We present evidence that there are gender differences in the neural mechanisms underlying emotion processes, and a likely interpretation is that males and females use different strategies during emotion processing, which may lead to gender differences in observed (or subjectively reported) processing of emotion (the emotion process). We discuss how these findings may offer insight into the mechanisms underlying gender differences in emotional behaviors, and outline a number of methodological factors that should be taken into consideration when interpreting this field of research.

Substantial evidence suggests that rumination is an important vulnerability factor for adolescent depression. Despite this, few studies have examined environmental risk factors that might lead to rumination and, subsequently, depression in adolescence. This study examined the hypothesis that an adverse family environment is a risk factor for rumination, such that the tendency to ruminate mediates the longitudinal association between a negative family environment and adolescent depressive symptoms. It also investigated adolescent gender as a moderator of the relationship between family environment and adolescent rumination. Participants were 163 mother-adolescent dyads. Adolescents provided self-reports of depressive symptoms and rumination across three waves of data collection (approximately at ages 12, 15, and 17 years). Family environment was measured via observational assessment of the frequency of positive and aggressive parenting behaviors during laboratory-based interactions completed by mother-adolescent dyads, collected during the first wave. A bootstrap analysis revealed a significant indirect effect of low levels of positive maternal behavior on adolescent depressive symptoms via adolescent rumination, suggesting that rumination might mediate the relationship between low levels of positive maternal behavior and depressive symptoms for girls. This study highlights the importance of positive parenting behaviors as a possible protective factor against the development of adolescent rumination and, subsequently, depressive symptoms. One effective preventive approach to improving adolescent mental health may be providing parents with psychoeducation concerning the importance of pleasant and affirming interactions with their children.

Introduction It is well established that childhood maltreatment has a detrimental impact on the brain, particularly the hippocampus. However, the hippocampus is a functionally and structurally heterogeneous region, and little is known about how maltreatment might affect hippocampal subregion development throughout important periods of plasticity. This study investigated whether childhood maltreatment was associated with the development of hippocampal subregion volumes from early to late adolescence. It also investigated associations between onset of psychiatric disorder and hippocampal subregion volume development. Methods One hundred and sixty-six (85 male) adolescents took part in three magnetic resonance imaging assessments during adolescence (mean age at each assessment: 12.79 [SD 0.43] years, 16.70 [SD 0.52] years, and 19.08 [SD 0.46] years), provided a self-report of childhood maltreatment, and were assessed for Axis I psychopathology. Results Childhood maltreatment was associated with the development of right total and left cornu ammonis 4 (CA4-DG) volumes from early to late adolescence. Early and late onset psychopathology was associated with the development of right presubiculum and right cornu ammonis 1 (CA1) volumes, respectively. Maltreatment findings appeared to be specific to males, whereas psychopathology findings appeared to be specific to females. Conclusions These findings provide evidence for possible deleterious effects of childhood maltreatment and early onset psychiatric disorder on the development of different subregions of the hippocampus. Altered development of the right CA1, on the other hand, might precede the development of late-adolescent onset psychopathology. Our results highlight the importance of considering development in research examining associations between stress, mental illness, and hippocampal morphology.

Background Adolescence is characterized by increasing prevalence of depressive symptomatology, along with significant structural brain development. While much research has examined focal abnormalities in gray matter structure underlying depression, we employed a structural coupling approach to examine whether longitudinal associations between amygdala and cortical development (referred to as maturational coupling) was related to concurrent changes in depressive symptomatology during adolescence. Method 166 participants underwent up to three MRI scans (367 scans) between 11 and 20 years of age. Depressive symptoms were measured at three coinciding time points using the Center for Epidemiological Studies-Depression scale. Linear mixed models were employed to identify whether change in amygdala volume was related to development of cortical thickness, and if maturational coupling of these regions was related to changes in depressive symptomatology. Results Positive maturational coupling was identified between the right amygdala and (predominantly anterior) prefrontal cortex, as well as parts of the temporal cortices. Greater positive coupling of these regions was associated with reductions in depressive symptoms over time. Conclusions Findings highlight significant associations between cortico-amygdalar maturational coupling and the emergence of depressive symptoms during adolescence, suggesting that synchronous development of these regions might support more adaptive affect regulation and functioning.

Major depression is a debilitating condition characterised by diverse neurocognitive and behavioural deficits. Nevertheless, our species-typical capacity for depressed mood implies that it serves an adaptive function. Here we apply an interdisciplinary theory of brain function to explain depressed mood and its clinical manifestations. Combining insights from the free-energy principle (FEP) with evolutionary theorising in psychology, we argue that depression reflects an adaptive response to perceived threats of aversive social outcomes (e.g., exclusion) that minimises the likelihood of surprising interpersonal exchanges (i.e., those with unpredictable outcomes). We suggest that psychopathology typically arises from ineffectual attempts to alleviate interpersonal difficulties and/or hyper-reactive neurobiological responses to social stress (i.e., uncertainty), which often stems from early experience that social uncertainty is difficult to resolve.

Social relationships promote health and wellbeing. Brain regions regulating social behavior continue to develop throughout adolescence, as teens learn to navigate their social environment with increasing sophistication. Adolescence is also a time of increased risk for the development of psychiatric disorders, many of which are characteristically associated with social dysfunction. In this review, we consider the links between adolescent brain development and the broader social environment. We examine evidence that individual differences in social ability, partly determined by genetic influences on brain structure and function, impact the quality and quantity of social ties during adolescence and that, conversely, the structure of one's social network exerts complex yet profound influences on individual behavior and mental health. In this way, the brain and social environment sculpt each other throughout the teenage years to influence one's social standing amongst peers. Reciprocal interactions between brain maturation and the social environment at this critical developmental stage may augment risk or promote resilience for mental illness and other health outcomes.

The cognitive regulation of emotion is impaired in major depressive disorder and has been linked to an imbalance of pre-frontal–subcortical brain activity. Despite suggestions that this relationship represents a neurodevelopmental marker of depression, few studies have examined the neural correlates of emotion regulation in depressed youth. We combined a ‘cognitive reappraisal’ paradigm with functional magnetic resonance imaging to study the neural correlates of emotional regulation in a large sample of non-medicated depressed adolescents and young adults (n = 53) and healthy controls (n = 64). As compared with healthy controls, young people with depression were less able to reduce negative affect during reappraisal, which corresponded to blunted modulation of amygdala activity. While in healthy individuals amygdala activation was modulated by age, no such relationship was observed in depressed individuals. Heightened activation of the ventromedial pre-frontal cortex (vmPFC) and reduced activation of the dorsal midline cortex was also found for the depressed group. Overall, these findings suggest that brain systems that support cognitive reappraisal are functionally altered in youth depression. We argue that excessive engagement of the vmPFC in particular, may be central to understanding how the process of putting a ‘positive spin’ on negative emotional material may be altered in depressed youth.

Variations in symptom trajectories within a population may represent distinct groups with different etiologies and outcomes. This study aimed to identify subgroups of depression symptom trajectories in a sample of adolescents, and to describe psychosocial attributes of the different groups. In a longitudinal study, 243 adolescents (121 males and 122 females), were assessed using a battery of measures of temperament, psychopathology, and psychological and behavioral functioning. Four phases of data collection over 7 years spanned average ages of the participants from 12 to 18 years old. Depressive symptoms from each phase were used to model latent class growth trajectories. A 4-group solution was selected as the best-fitting model: (1) ongoing stable low levels of depression; (2) very high depressive symptoms initially, but a steep decrease in symptoms over time; (3) moderately high depressive symptoms initially, but symptoms decreased over time; and (4) initially low levels of symptoms that increased over time. Trajectory group membership was associated with a range of psychosocial variables including temperament, childhood maltreatment, and young adult quality of life. Characterising these subgroups allows for a better understanding of how the interaction of risk factors increases the likelihood of depression and other poor outcomes, and highlights the importance of early interventions to prevent and treat adolescent depression.

Background Schizophrenia is thought to be a neurodevelopmental disorder with pathophysiological processes beginning in the brain prior to the emergence of clinical symptoms. Recent evidence from neuroimaging studies using techniques such as diffusion tensor imaging has identified white matter abnormalities that are suggestive of disrupted brain myelination and neuronal connectivity. Identifying whether such effects exist in individuals at high risk for developing psychosis may help with prevention and early intervention strategies. In addition, there is preliminary evidence for a role of lipid biology in the onset of psychosis, along with well-established evidence of its role in myelination of white matter tracts. As such, this article synthesises the literature on polyunsaturated fatty acids (PUFAs) in myelination and schizophrenia, hypothesizing that white matter abnormalities may potentially mediate the relationship between PUFAs and schizophrenia. Methods Diffusion tensor imaging studies were identified through a systematic search of existing literature. Studies examined white matter integrity in ultra-high risk (UHR) samples, as assessed using structured diagnostic interviews. Data was extracted and summarised as a narrative review. Results Twelve studies met inclusion criteria, and findings identified reduced fractional anisotropy and higher diffusivity. Although the exact location of abnormalities remains uncertain, fronto-temporal and fronto-limbic connections, including the superior longitudinal and uncinate fasiculus, cingulum, and corpus callosum appear to be implicated. Because of preliminary evidence suggesting lipid biology may be relevant for the onset of psychosis, a discussion is provided of the role of polyunsaturated fatty acids (PUFAs) in myelination and risk for psychosis. Conclusions While the function of PUFAs in myelination is well-established, there is growing evidence of reduced PUFA concentration in UHR samples, highlighting the need for research to examine the relationship between PUFA and white matter integrity in high-risk samples and age-matched healthy controls. Such investigations will help to better understand the pathophysiology of the disorder, and potentially assist in the development of novel treatment and early intervention strategies.

High levels of depression during adolescence may contribute to the risk for future depression later in life. This study examined the relationship between the developmental timing of depressive symptoms, and brain structural outcomes in late adolescence. In a prior work, we examined longitudinal trajectories of depressive symptoms in 243 adolescents (121 males and 122 females), and identified four subgroups: a normative group with stable low levels of depression, two groups with declining symptoms, and one group with increasing symptoms. For the current paper, diffusion-weighted MRI images were acquired at the final wave of the study, and used to perform white matter tractography and brain network analysis. The four depression trajectory groups were tested for differences in brain connectivity variables. This revealed differences in several frontal and temporal regions. The groups that had experienced elevated depression symptoms in early adolescence differed from the normative group in a greater number of areas than the group who had experienced depression later. Affected tracts corresponded to areas of white matter that are still maturing during this period, particularly frontolimbic regions. These findings support the proposition that the timing and duration of depression symptoms during adolescence are associated with brain structural outcomes.

Aims: The study aimed to investigate childhood maltreatment, sex, and borderline personality disorder (BPD) symptoms as prospective predictors of adolescent hypothalamic-pituitary-adrenal (HPA) axis reactivity. Method: A sample of 69 adolescents (30 female and 39 male) were selected from a larger longitudinal study of adolescent development and assessed at 3 time points. BPD symptoms were assessed at T1 (approx. 12.5 years), childhood maltreatment was assessed at T2 (approx. 14.9 years), and multiple assessments of salivary cortisol (cortisol awakening response; CAR) were undertaken at T3 (approx. 15.5 years). Results: Multivariate linear regression analysis revealed a significant main effect for childhood maltreatment but not for early BPD symptoms as a predictor of lower CAR in adolescence (p = 0.047). The association between childhood maltreatment and attenuated CAR was moderated by both early BPD symptoms (p = 0.024; no childhood maltreatment-dependent attenuation of CAR in the presence of BPD symptoms) and sex (p = 0.012; childhood maltreatment-dependent attenuation of CAR in females only). Furthermore, a 3-way BPD × childhood maltreatment × sex interaction (p = 0.041) indicated that the moderating effect of BPD symptoms was present in females only. Conclusion: These findings indicate that attenuation of the HPA axis occurs as a response to early maltreatment rather than being related to the early occurrence of BPD pathology. Traumatized female individuals with BPD symptoms might bypass adaptive HPA axis attenuation.

This study conducted a systematic review to synthesize findings on the development of functional and structural brain networks from the prenatal to late adolescent period. In addition, evidence for environmental and genetic influences on the development of brain networks was reviewed. Ninety two studies fulfilled the inclusion criteria. Diffusion MRI findings indicated that clustering decreases, local and global efficiency increase and modularity stabilizes or decreases with age. Structural covariance findings indicated that local efficiency, global efficiency and modularity, may stabilize in adolescence. Findings for resting-state functional MRI were mixed. Few studies have investigated genetic or environmental influences on development of structural or functional networks. For functional networks, genetic effects have been reported with few significant environmental factors. While no studies of this nature were found for structural networks, other research has provided evidence of age-related changes in heritability of white matter volume, fractional anisotropy, and cortical thickness. Further research is required to understand the development of brain networks and the relevance of environmental and genetic factors.

Early timing of puberty (i.e., advanced pubertal maturation relative to peers) has been linked to the onset of depressive symptoms during the early adolescent phase. However, the precise neurobiological mechanisms linking early pubertal timing to adolescent depressive symptoms are not clear. We investigated whether the volume of the pituitary gland, a key component of the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal (HPA) axes, mediated the relationship between pubertal timing and depressive symptoms in 155 adolescents (72 females) both cross-sectionally and longitudinally. At baseline (M age 12.7, SD 0.5 years), early pubertal timing predicted larger pituitary gland volume and higher depressive symptoms (especially for girls), but there was no mediation effect. Longitudinally, however, larger pituitary gland volume at baseline was found to mediate the relationship between early pubertal timing and increased depressive symptoms over time (M follow-up period=2.57 years, SD=0.26) for both boys and girls. Our findings suggest that neurobiological mechanisms are partly responsible for the link between early pubertal timing and depressive symptoms in adolescents. We speculate that an enlarged pituitary gland in adolescents with early pubertal timing might be associated with hyperactivation of the hormonal stress response, leading to increased susceptibility to environmental stressors, and subsequent development of depressive symptoms. Given the well-established relationship between increasing depressive symptoms in adolescence and later disorder, these findings have implications for targeted prevention and early intervention strategies for depressive disorders in adolescence.

Objective: Inhibitory control is associated with temperament and intelligence, which together form an essential component of the ability to adaptively regulate behavior. Impairments in inhibitory control have been linked with a host of common and debilitating conditions, often in a sex-dependent manner. However, sex differences in inhibitory control are often not expressed experimentally during task performance. Here, we sought to examine how sex, temperament, and intelligence are related to different aspects of inhibitory control. Method: We recruited a large sample of early adolescents (n = 153; mean age 12.6 years) to comprehensively investigate the relationship between sex, self-reported and parent-reported temperamental effortful control, and intelligence with different aspects of inhibitory control-namely, strategic (or proactive) control and evaluative (or reactive) control, assessed using a modified Stroop task. Results: Compared with males, females were more efficient in their use of strategic control to reduce the magnitude of response conflict. There was no sex difference in evaluative control. Further, whereas high intelligence was associated with fewer errors for both males and females, effortful control was associated with performance accuracy only in females. Conclusions: These findings highlight sex differences in the relationship of inhibitory control to individual differences in temperamental effortful control in early adolescents and reinforce the generalized positive effects of intelligence. (PsycINFO Database Record (c) 2012 APA, all rights reserved). Language: en

Background There is growing evidence that long-term, heavy cannabis use is associated with alterations in regional brain volumes. Although these changes are frequently attributed to the neurotoxic effects of cannabis, it is possible that some abnormalities might predate use and represent markers of vulnerability. To date, no studies have examined whether structural brain abnormalities are present before the onset of cannabis use. This study aims to determine whether adolescents who have initiated cannabis use early (i.e., before age 17 years) show premorbid structural abnormalities in the amygdala, hippocampus, orbitofrontal cortex, and anterior cingulate cortex. Methods Participants ( n = 121) were recruited from primary schools in Melbourne, Australia, as part of a larger study examining adolescent emotional development. Participants underwent structural magnetic resonance imaging at age 12 years and were assessed for cannabis use 4 years later, at age 16 years. At the follow-up assessment, 28 participants had commenced using cannabis (16 female subjects [57%]), and 93 had not (43 female subjects [46%]). Results Smaller orbitofrontal cortex volumes at age 12 years predicted initiation of cannabis use by age 16 years. The volumes of other regions (amygdala, hippocampus, and anterior cingulate cortex) did not predict later cannabis use. Conclusions These findings suggest that structural abnormalities in the orbitofrontal cortex might contribute to risk for cannabis exposure. Although the results have important implications for understanding neurobiological predictors of cannabis use, further research is needed to understand their relationship with heavier patterns of use in adulthood as well as later abuse of other substances.

The way that parents express their emotions during interactions with their adolescent children is important for adolescent adjustment, and predicts adolescent emotional problems such as depression. In the current study, we assessed whether adolescent depressive symptoms were associated with neural activity during exposure to their mother's affective behavior. Thirty adolescents (18 females, mean age 17.35, s.d. 0.43) participated in an fMRI task that used digitized video segments of their own mother's, as well as an unfamiliar mother's affective behavior as stimuli. Exposure to one's own (compared to an unfamiliar) mother's positive (compared to neutral) behavior was associated with activation in the anterior and posterior cingulate, precuneus and ventrolateral prefrontal cortex. In contrast, exposure to positive behavior across own and an unfamiliar mother (controlling for neutral behavior) was associated with superior temporal sulcus, occipital pole, amygdala and striatum activity. Adolescent depressive symptoms were associated with reduced rostral anterior cingulate activity during exposure to one's own (compared to an unfamiliar) mother's positive behavior, and reduced striatal activity during exposure to positive behavior in general. This study represents an important step in furthering our understanding of the neural basis of affective processing in adolescents. Further, the results support a disruption of reward function in depression.

BackgroundThe cerebellum is rich in cannabinoid receptors and implicated in the neuropathology of schizophrenia. Long-term cannabis use is associated with functional and structural brain changes similar to those evident in schizophrenia, yet its impact on cerebellar structure has not been determined. We examined cerebellar grey and white matter in cannabis users with and without schizophrenia.MethodSeventeen patients with schizophrenia and 31 healthy controls were recruited; 48% of the healthy group and 47% of the patients were long-term heavy cannabis users (mean 19.7 and 17.9 years near daily use respectively). Cerebellar measures were extracted from structural 3-T magnetic resonance imaging (MRI) scans using semi-automated methods, and examined using analysis of covariance (ANCOVA) and correlational analyses.ResultsCerebellar white-matter volume was reduced in cannabis users with and without schizophrenia compared to healthy non-users, by 29.7% and 23.9% respectively, and by 17.7% in patients without cannabis use. Healthy cannabis users did not differ in white-matter volume from either of the schizophrenia groups. There were no group differences in cerebellar grey matter or total volumes. Total cerebellar volume decreased as a function of duration of cannabis use in the healthy users. Psychotic symptoms and illness duration correlated with cerebellar measures differentially between patients with and without cannabis use.ConclusionsLong-term heavy cannabis use in healthy individuals is associated with smaller cerebellar white-matter volume similar to that observed in schizophrenia. Reduced volumes were even more pronounced in patients with schizophrenia who use cannabis. Cannabis use may alter the course of brain maturational processes associated with schizophrenia.

It has been suggested that biological factors confer increased sensitivity to environmental influences on depressive symptoms during adolescence, a crucial time for the onset of depressive disorders. Given the critical role of the hippocampus in sensitivity to stress and processing of contextual aspects of the environment, investigation of its role in determining sensitivity to environmental context seems warranted. This study prospectively examined hippocampal volume as a measure of sensitivity to the influence of aggressive maternal behavior on change in depressive symptoms from early to midadolescence. The interaction between aggressive maternal behavior and hippocampal volume was found to predict change in depressive symptoms. Significant sex differences also emerged, whereby only for girls were larger bilateral hippocampal volumes more sensitive to the effects of maternal aggressive behavior, particularly with respect to experiencing the protective effects of low levels of maternal aggressiveness. These findings help elucidate the complex relationships between brain structure, environmental factors such as maternal parenting style, and sensitivity to (i.e., risk for, and protection from) the emergence of depression during this life stage. Given that family context risk factors are modifiable, our findings suggest the potential utility of targeted parenting interventions for the prevention and treatment of adolescent depressive disorder.

Background: Early adolescence is a critical time for the development of both internalizing and externalizing disorders. We aimed to investigate whether pituitary volume, an index of hypothalamic–pituitary–adrenal (HPA) axis function, represents a vulnerability factor for the emergence of internalizing and externalizing symptoms during adolescence using a prospective, longitudinal design. Methods: One hundred and fifty‐five adolescents completed 3T structural magnetic resonance imaging (MRI), symptom rating scales and a diagnostic interview during early adolescence (M age 12.6 years, SD .5 years); symptom rating scales were re‐administered approximately three years later (M age 15.2 years). The volume of the pituitary gland was estimated by manually delineating its structure on MR images. The degree to which pituitary volumes prospectively predicted change in internalizing and externalizing symptoms across the two time‐points was assessed using hierarchal linear regression, after controlling for the influence of gender, age, pubertal stage and intracranial volume. Results: Larger pituitary volumes prospectively predicted an increase in internalizing, but not externalizing, symptoms from early adolescence to mid‐adolescence. Conclusions: This study provides the first evidence that increased pituitary volume might represent a specific vulnerability marker for the development of internalizing symptoms during early to mid‐adolescence.

Objective Parenting and pubertal timing have consistently been associated with internalizing and externalizing symptoms in childhood and adolescence, and there is some evidence that the interaction between these factors may be important in conferring risk. However, few studies have investigated whether neurobiological factors mediate these relationships. The current study examined whether interactions between adrenarcheal timing and parenting styles were associated with affective brain function and, in turn, mental health difficulties. Method Participants were 88 healthy children (46 female and 42 male, mean age 9.42 years, SD = 1.08 years), with 45 classified as relatively early and 43 as relatively late in adrenarcheal development based upon adrenal hormone levels. Participants completed an affective face functional magnetic resonance imaging task, and parents reported on 5 parenting styles and on child internalizing and externalizing symptoms. Results Negative parenting styles (corporal punishment and poor monitoring) were associated with brain hemodynamic response while viewing affective faces in several subcortical and lateral prefrontal regions, and adrenarcheal timing and/or sex moderated most of these relationships. Sex differences in associations between corporal punishment and brain activation to affective faces indicated that late females might show less adaptive affective neural function when more exposed to this parenting style. Conclusion Findings suggest that the interaction between parenting styles and adrenarcheal timing is associated with affective brain function in late childhood, with marked sex differences. Further longitudinal research with larger samples is needed to corroborate and expand upon these findings.

Reports of volumetric abnormalities in the anterior cingulate cortex (ACC) in adults with established borderline personality disorder (BPD) are inconsistent, and it is not known whether such abnormalities are present early in the disorder. We aimed to investigate ACC volume in a first-presentation teenage BPD sample with minimal exposure to treatment. Fifteen female BPD patients and 15 healthy female control participants underwent magnetic resonance imaging (MRI) scanning. ACC volumes were estimated using a reliable method that accounts for inter-individual variation in sulcal morphology, and measurements were compared between the two groups. Analysis of variance revealed a decrease in volume of the left ACC in BPD patients compared with control participants. This volumetric change was correlated with parasuicidal behavior and impulsivity. A measure of ACC volume asymmetry was also correlated with fear of abandonment symptoms. Our results suggest that ACC volumetric abnormalities early in the course of BPD might be related to clinical correlates of the disorder. Longitudinal studies are needed to examine the nature of this abnormality over the course of the disorder.

The development of reward-based learning and decision-making, and the neural circuitry underlying these processes, appears to be influenced negatively by adverse child-rearing environments characterized by abuse and other forms of maltreatment. No research to-date has investigated whether normative variations in the child-rearing environment have effects on adolescent brain structure. We examined whether normative variations in maternal responses to adolescents’ positive affective behavior were associated with morphometric measures of the adolescents’ affective neural circuitry, namely the amygdala, orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC). Healthy adolescents (N = 113) participated in laboratory-based interaction tasks with their mothers, and underwent high-resolution (3T) structural magnetic resonance imaging (MRI). The mother–adolescent interactions included a pleasant event-planning interaction (EPI) and a conflictual problem-solving interaction (PSI). Adolescents, whose mothers displayed more punishing responses to their positive affective behavior during both tasks, and only during the PSI, had larger left dorsal ACC and bilateral OFC volumes, respectively. In addition, boys whose mothers evidenced this pattern of behavior during the EPI had larger right amygdala volumes. These results suggest that normative variations in maternal responses to affective behavior are associated with the structural characteristics of adolescents’ affective neural circuitry, which may have implications for the development of their social, cognitive and affective functioning.

Adolescence is a key period for the development of brain circuits underlying affective and behavioral regulation. It remains unclear, however, whether and how adolescent brain structure influences day-to-day affective behavior. Because of significant changes in the nature of family relations that also typically occur during adolescence, parent–child interactions provide a meaningful context where affective behavior and its regulation may be assessed. In a sample of 137 early adolescents, we investigated the relationship between aspects of the adolescents' brain structure and their affective behavior as assessed during observation of parent–child interactions. We found a significant positive association between volume of the amygdala and the duration of adolescent aggressive behavior during these interactions. We also found male-specific associations between the volume of prefrontal structures and affective behavior, with decreased leftward anterior paralimbic cortex volume asymmetry associated with increased duration of aggressive behavior, and decreased leftward orbitofrontal cortex volume asymmetry associated with increased reciprocity of dysphoric behavior. These findings suggest that adolescent brain structure is associated with affective behavior and its regulation in the context of family interactions, and that there may be gender differences in the neural mechanisms underlying affective and behavioral regulation during early adolescence. Particularly as adolescence marks a period of rapid brain maturation, our findings have implications for mental health outcomes that may be revealed later along the developmental trajectory.

The structural and functional consequences of interindividual variations in cortical morphology are poorly understood. In this study, we examined the relationship between one well‐characterized variation of the medial frontal lobes, variability of the paracingulate sulcus (PCS), and grey matter volume, cortical thickness, surface area, and sulcal depth of the adjacent anterior cingulate cortex (ACC) and paracingulate cortex (PaC). Seventy‐seven healthy individuals were assigned to one of four groups depending on PCS incidence in both hemispheres: left‐present, right‐absent; left‐absent, right‐present; both absent; or both present. Comparing these groups on each measure yielded four primary findings: (1) The presence of a PCS was associated with increased PaC and decreased ACC grey matter volume in the hemisphere in which it was apparent, with an almost identical pattern being observed for surface area; (2) there was a more complex relationship between PCS variability and regional thickness, such that a PCS in the left hemisphere was associated with increased left PaC and right ACC thickness, with no comparable effects being observed for the presence of a right PCS; (3) the depths of all major left hemisphere sulci in the region were strongly positively correlated, whereas no such associations were apparent in the right hemisphere; and (4) a leftward asymmetry in PaC thickness was specifically associated with better performance on a test of spatial working memory ability. These results provide evidence for a complex interhemispheric relationship between sulcal variability and cortical morphometry, and indicate that such relationships may be important for understanding individual differences in cognitive abilities. Hum Brain Mapp, 2008. © 2007 Wiley‐Liss, Inc.

Olfactory deficits have been reported in major depressive disorder (MDD). However, it remains largely unknown whether MDD is associated with abnormalities in olfactory sulcus morphology, a potential marker of olfactory system development. This magnetic resonance imaging study investigated the length and depth of the olfactory sulcus in 29 currently depressed patients, 27 remitted depressed patients, and 33 age- and gender-matched healthy control subjects. Both current and remitted MDD patients had significantly shallower olfactory sulci bilaterally as compared with controls. Only for male subjects, the right olfactory sulcus was significantly shorter in remitted MDD patients than in controls. The right sulcus depth was negatively correlated with number of depressive episodes in the entire MDD group and with residual depressive symptoms in the remitted MDD group. Medication status, presence of melancholia, and comorbidity with anxiety disorders did not affect the sulcus morphology. These findings suggest that abnormality of the olfactory sulcus morphology, especially its depth, may be a trait-related marker of vulnerability to major depression.

Adolescence is a time when the ability to consciously control thoughts, actions, and emotions is linked to successful outcomes later in life. Despite a historical focus on the prefrontal cortex, modern neuroimaging research suggests that these cognitive control abilities are mediated by the activity and interactions of brain regions that collectively form distributed networks. This chapter outlines research and methods that have highlighted the importance of brain network dynamics (i.e., the spatiotemporal interactions between brain regions) during cognitive control in adolescence. On the basis of current research, we suggest that transient reconfigurations of brain networks that occur in specific contexts are critical to cognitive control in adolescence. In particular, we suggest that the spatiotemporal dynamics of brain networks play a crucial role in governing adolescent cognitive control across different contexts (i.e., they are generalizable). We suggest that further research of generalizable principles will help adolescents with low cognitive control.

The human brain undergoes substantial development throughout adolescence and into early adulthood. This maturational process is thought to include the refinement of connectivity between putative connectivity hub regions of the brain, which collectively form a dense core that enhances the functional integration of anatomically distributed, and functionally specialized, neural systems. Here, we used longitudinal diffusion magnetic resonance imaging to characterize changes in connectivity between 80 cortical and subcortical anatomical regions over a 2 year period in 31 adolescents between the ages of 15 and 19 years. Connectome-wide analysis indicated that only a small subset of connections showed evidence of statistically significant developmental change over the study period, with 8% and 6% of connections demonstrating decreased and increased structural connectivity, respectively. Nonetheless, these connections linked 93% and 90% of the 80 regions, respectively, pointing to a selective, yet anatomically distributed pattern of developmental changes that involves most of the brain. Hub regions showed a distinct tendency to be highly connected to each other, indicating robust "rich-club" organization. Moreover, connectivity between hubs was disproportionately influenced by development, such that connectivity between subcortical hubs decreased over time, whereas frontal-subcortical and frontal-parietal hub-hub connectivity increased over time. These findings suggest that late adolescence is characterized by selective, yet significant remodeling of hub-hub connectivity, with the topological organization of hubs shifting emphasis from subcortical hubs in favor of an increasingly prominent role for frontal hub regions.

Adversity early in life can disrupt the functioning of the hypothalamic-pituitary-adrenal axis (HPAA) and increase risk for negative health outcomes. Recent research suggests that cortisol in scalp hair represents a promising measure of HPAA function. However, little is known about the relationship between early exposure to traumatic events and hair cortisol concentrations (HCC) in childhood, a critical period of HPAA development. The current study measured HCC in scalp hair samples collected from 70 community-based children (14 males, mean age=9.50) participating in the Imaging Brain Development in the Childhood to Adolescence Transition Study (iCATS). Data were also collected on lifetime exposure to traumatic events and current depressive symptoms. Lifetime exposure to trauma was associated with elevated HCC; however, HCC was not associated with current depressive symptoms. Consistent with some prior work, males were found to have higher HCC than females, although results should be treated with caution due to the small number of males who took part. Our findings suggest that hair cortisol may represent a biomarker of exposure to trauma in this age group; however, further study is necessary with a particular focus on the characterization of trauma and other forms of adversity.

Few studies have examined the neural correlates of emotion regulation across adolescence and young adulthood. Existing studies of cognitive reappraisal indicate that improvements in regulatory efficiency may develop linearly across this period, in accordance with maturation of prefrontal cortical systems. However, there is also evidence for adolescent differences in reappraisal specific to the activation of “social‐information processing network” regions, including the amygdala and temporal‐occipital cortices. Here, we use fMRI to examine the neural correlates of emotional reactivity and reappraisal in response to aversive social imagery in a group of 78 adolescents and young adults aged 15–25 years. Within the group, younger participants exhibited greater activation of temporal‐occipital brain regions during reappraisal in combination with weaker suppression of amygdala reactivity—the latter being a general correlate of successful reappraisal. Further analyses demonstrated that these age‐related influences on amygdala reactivity were specifically mediated by activation of the fusiform face area. Overall, these findings suggest that enhanced processing of salient social cues (i.e., faces) increases reactivity of the amygdala during reappraisal and that this relationship is stronger in younger adolescents. How these relationships contribute to well‐known vulnerabilities of emotion regulation during this developmental period will be an important topic for ongoing research. Hum Brain Mapp 37:7–19, 2016. © 2015 Wiley Periodicals, Inc.

The parent-adolescent relationship is an important predictor of adolescent mental health, especially depressive disorders. This relationship is constructed in the context of maturing emotion neurobiology and could help shape such neurobiology in ways that are important for current and future mental health. Amygdala resting-state functional networks have been linked to depression, but whether such resting connectivity is associated with parent affective behaviors or acts as a salient mediator between parenting and risk for depressive disorder is unknown.In the present study of 128 individuals, a 7-year longitudinal design was used to examine how observed maternal aggressive behavior during mother-adolescent interactions in early adolescence (12 years) predicted amygdala (whole and subregion)-based resting connectivity in mid adolescence (16 years). In 101 of those participants, whether altered amygdala resting-state connectivity mediated the association between maternal aggressive behavior and the first onset of major depressive disorder (MDD) in late adolescence (19 years) was analyzed.Maternal aggression was related to resting-state functional connectivity between the amygdala and right superior temporal-posterior insula-Heschl gyri, bilateral visual cortex, and left temporal and insula cortices (the latter being driven by the centromedial amygdala subregion; p .001). Further, amygdala and centromedial amygdala connectivity with the temporal and insula cortices mediated the association between maternal aggression and late adolescent-onset MDD (CI 0.20 to 2.87; CI 0.13 to 2.40, respectively).These findings are consistent with previous literature documenting the importance of amygdala resting networks for adolescent depression but further suggest the importance of parental affective (particularly aggressive) behavior in the development of such functional connectivity patterns during this period of peak onset for mental health disorders.