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Unstable and unpredictable environments are linked to risk for psychopathology, but the underlying neural mechanisms that explain how instability relate to subsequent mental health concerns remain unclear. In particular, few studies have focused on the association between instability and white matter structures despite white matter playing a crucial role for neural development. In a longitudinal sample recruited from a population-based study (N = 237), household instability (residential moves, changes in household composition, caregiver transitions in the first 5 years) was examined in association with adolescent structural network organization (network integration, segregation, and robustness of white matter connectomes; M age = 15.87) and young adulthood anxiety and depression (six years later). Results indicate that greater instability related to greater global network efficiency, and this association remained after accounting for other types of adversity (e.g., harsh parenting, neglect, food insecurity). Moreover, instability predicted increased depressive symptoms via increased network efficiency even after controlling for previous levels of symptoms. Exploratory analyses showed that structural connectivity involving the left fronto-lateral and temporal regions were most strongly related to instability. Findings suggest that structural network efficiency relating to household instability may be a neural mechanism of risk for later depression and highlight the ways in which instability modulates neural development. [ABSTRACT FROM AUTHOR]

Social deficits in autism spectrum disorder (ASD) are linked to amygdala functioning and functional connection between the amygdala and subgenual anterior cingulate cortex (sACC) is involved in the modulation of amygdala activity. Impairments in behavioral symptoms and amygdala activation and connectivity with the sACC seem to vary by serotonin transporter-linked polymorphic region (5-HTTLPR) variant genotype in diverse populations. The current preliminary investigation examines whether amygdala-sACC connectivity differs by 5-HTTLPR genotype and relates to social functioning in ASD. A sample of 108 children and adolescents (44 ASD) completed an fMRI face-processing task. Youth with ASD and low expressing 5-HTTLPR genotypes showed significantly greater connectivity than youth with ASD and higher expressing genotypes as well as typically developing (TD) individuals with both low and higher expressing genotypes, in the comparison of happy vs. baseline faces and happy vs. neutral faces. Moreover, individuals with ASD and higher expressing genotypes exhibit a negative relationship between amygdala-sACC connectivity and social dysfunction. Altered amygdala-sACC coupling based on 5-HTTLPR genotype may help explain some of the heterogeneity in neural and social function observed in ASD. This is the first ASD study to combine genetic polymorphism analyses and functional connectivity in the context of a social task. [ABSTRACT FROM AUTHOR]

• Amygdala-PFC connections in ASD vs TD differ in a socio-emotional faces task and rest. • Amygdala-insula/temporal connectivity patterns persist regardless of context in ASD. • The role of context is an important future direction for social impairment research. The amygdala-prefrontal cortex circuit is involved in processing socio-emotional cues and may partially mediate social impairment in autism spectrum disorder (ASD). Past task-based fMRI studies in ASD indicate a mix of hypo- and hyper-connectivity in response to socio-emotional stimuli whereas resting state studies report hypoconnectivity between these regions. However, it is still unknown whether ASD-related alterations in amygdala-prefrontal circuitry are present across socio-emotional tasks and resting state contexts within the same sample or instead, depend on con. ASD (n = 47) and typically developing individuals (TD; n = 72) underwent fMRI during an implicit emotional face processing task and during rest, and whole-brain amygdala connectivity was calculated to determine patterns that differed by context and diagnosis. Relative to TD, the ASD group demonstrated weaker left amygdala connectivity with the medial frontal gyrus and the left superior frontal gyrus during rest, but stronger connectivity during task. Furthermore, across both contexts, ASD vs. TD had stronger right amygdala connectivity with the left insula/superior temporal gyrus. Findings suggest some alterations in amygdala connectivity of ASD may depend on context while others are pervasive across task and rest conditions. Understanding context-dependent brain alterations in ASD may help disambiguate the mechanisms subserving social impairment and provide targets for treatment. [ABSTRACT FROM AUTHOR]

Biased attention to threat represents a key feature of anxiety disorders. This bias is altered by therapeutic or stressful experiences, suggesting that the bias is plastic. Charting on-line behavioral and neurophysiological changes in attention bias may generate insights on the nature of such plasticity. We used an attention-orientation task with threat cues to examine how healthy individuals alter their response over time to such cues. In Experiments 1 through 3, we established that healthy individuals demonstrate an increased attention bias away from threat over time. For Experiment 3, we used functional magnetic resonance imaging to determine the neural bases for this phenomenon. Gradually increasing attention bias away from threat is associated with increased activation in the occipitotemporal cortex. Examination of plasticity of attention bias with individuals at risk for anxiety disorders may reveal how threatening stimuli come to be categorized differently in this population over time. [Copyright &y& Elsevier]

Background: Females appear to be more sensitive and responsive to social cues, including threat signals, than are males. Recent theoretical models suggest that developmental changes in brain functioning play important roles in the emergence of such gender differences.Methods: We used functional magnetic resonance imaging to examine developmental and gender differences in activation of neural structures thought to mediate attention to emotional faces depicting varying degrees of threat. Analyses focused on the orbitofrontal cortex, amygdala, and anterior cingulate cortex during the evaluation of threat conveyed by faces. Healthy adolescents (n = 17; 53% male) and adults (n = 17; 53% male) were scanned while they rated how threatening pictures of neutral and emotional (angry, fearful, or happy) faces appeared.Results: Results indicate significant interactions among age, gender, and face type for activation during explicit threat monitoring. In particular, adult women activated orbitofrontal cortex and amygdala selectively to unambiguous threat (angry) cues, while adult men showed a less discriminating pattern of activation. No gender differences were evident for adolescents, who as a group resembled adult males.Conclusions: These findings suggest that there are gender differences in patterns of neural responses to emotional faces that are not fully apparent until adulthood. [Copyright &y& Elsevier]

Childhood adversity is heterogeneous with potentially distinct dimensions of violence exposure and social deprivation. These dimensions may differentially shape emotion-based neural circuitry, such as amygdala–PFC white matter connectivity. Amygdala–orbitofrontal cortex (OFC) white matter connectivity has been linked to regulation of the amygdala's response to emotional stimuli. Using a preregistered analysis plan, we prospectively examined the effects of childhood exposure to two dimensions of adversity, violence exposure and social deprivation, on the adolescent amygdala–PFC white matter connectivity. We also reproduced the negative correlation between amygdala–PFC white matter connectivity and amygdala activation to threat faces. 183 15−17-year-olds were recruited from the Fragile Families and Child Wellbeing Study — a longitudinal, birth cohort, sample of predominantly low-income youth. Probabilistic tractography revealed that childhood violence exposure and social deprivation interacted to predict the probability of adolescent right hemisphere amygdala–OFC white matter connectivity. High violence exposure with high social deprivation related to less amygdala–OFC white matter connectivity. Violence exposure was not associated with white matter connectivity when social deprivation was at mean or low levels (i.e., relatively socially supportive contexts). Therefore, social deprivation may exacerbate the effects of childhood violence exposure on the development of white matter connections involved in emotion processing and regulation. Conversely, social support may buffer against them. [ABSTRACT FROM AUTHOR]

This article has been withdrawn: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been withdrawn at the request of the editor and publisher. The publisher regrets that an error occurred which led to the premature publication of this paper. This error bears no reflection on the article or its authors. The publisher apologizes to the authors and the readers for this unfortunate error. [ABSTRACT FROM AUTHOR]

Since the first neurodevelopmental models that sought to explain the influx of risky behaviors during adolescence were proposed, there have been a number of revisions, variations and criticisms. Despite providing a strong multi-disciplinary heuristic to explain the development of risk behavior, extant models have not yet reliably isolated neural systems that underlie risk behaviors in adolescence. To address this gap, we screened 2017 adolescents from an ongoing longitudinal study that assessed 15-health risk behaviors, targeting 104 adolescents (Age Range: 17-to-21.4), characterized as high-or-average/low risk-taking. Participants completed the Monetary Incentive Delay (MID) fMRI task, examining reward anticipation to "big win" versus "neutral". We examined neural response variation associated with both baseline and longitudinal (multi-wave) risk classifications. Analyses included examination of a priori regions of interest (ROIs); and exploratory non-parametric, whole-brain analyses. Hypothesis-driven ROI analysis revealed no significant differences between high- and average/low-risk profiles using either baseline or multi-wave classification. Results of whole-brain analyses differed according to whether risk assessment was based on baseline or multi-wave data. Despite significant mean-level task activation, these results do not generalize prior neural substrates implicated in reward anticipation and adolescent risk-taking. Further, these data indicate that whole-brain differences may depend on how risk-behavior profiles are defined. [ABSTRACT FROM AUTHOR]

Objective: Characterizing the pathophysiology of irritability symptoms from a dimensional perspective above and beyond diagnostic boundaries is key to developing mechanism-based interventions that can be applied broadly. Face emotion processing deficits are present in youths with elevated levels of irritability. The present study aimed to identify the neural mechanisms of face emotion processing in a sample enriched for irritability by including youths with high-functioning autism spectrum disorder (HF-ASD).Method: Youths (N = 120, age = 8.3-19.2 years) completed an implicit face emotion task during functional magnetic resonance imaging. We evaluated how irritability, measured dimensionally, above and beyond diagnostic group, relates to whole-brain neural activation and amygdala connectivity in response to face emotions.Results: Both neural activation and amygdala connectivity differed as a function of irritability level and face emotion in the prefrontal cortex. Youths with higher irritability levels had decreased activation in response to both fearful and happy faces in the left middle frontal gyrus and to happy faces in the left inferior frontal gyrus. Furthermore, increased irritability levels were associated with altered right amygdala connectivity to the left superior frontal gyrus when viewing fearful and sad faces.Conclusion: The neural mechanisms of face emotion processing differ in youths with higher irritability compared to their less irritable peers. The findings suggest that these irritability mechanisms may be common to both typically developing and HF-ASD youths. Understanding the neural mechanisms of pediatric irritability symptoms that cut across diagnostic boundaries may be leveraged for future intervention development. [ABSTRACT FROM AUTHOR]

Structural differences in the amygdala (AMG) are implicated in anxiety and observed among individuals with generalized (GAD) and social anxiety (SAD) disorders. Findings have been mixed, perhaps because studies rarely examine differences between GAD and SAD, test comorbidity, or examine age-related differences. We tested AMG volume differences among a sample of adults and youth with/without SAD and GAD. Participants (N = 242; ages 7–60 years) completed an MRI scan, diagnostic interviews, and anxiety symptom measures. Groups were formed from diagnostic interviews: 1) Typically developing (TD; n = 91); 2) GAD (n = 53); 3) SAD (n = 35); and 4) comorbid SAD/GAD (n = 63). We used analysis of covariance with a bonferroni correction to examine group differences in AMG volume. The SAD and comorbid SAD/GAD groups exhibited increased bilateral AMG volume compared to the TD group. GAD and TD groups did not differ from each other in AMG size. The SAD, but not the comorbid SAD/GAD group, displayed greater right AMG size relative to the GAD group. SAD and comorbid SAD/GAD groups did not differ from the GAD group in left AMG volume. SAD and SAD/GAD groups did not exhibit different bilateral AMG size. Linear regression analyses demonstrated that greater social anxiety but not generalized anxiety symptom severity was associated with enlarged AMG volume. Age was not associated with AMG volume and nor did age moderate any group or symptom effects. Future longitudinal studies should examine whether larger AMG volume is a unique biomarker for SAD across the lifespan. • Social anxiety disorder was linked with larger amygdala size across the lifespan. • Generalized anxiety and healthy individuals did not differ in amygdala size. • Comorbid social and generalized anxiety was associated with larger amygdala volume. • Greater social anxiety symptom severity was related to larger amygdala volume. • Results could enhance clinical prediction models of SAD risk and treatment response. [ABSTRACT FROM AUTHOR]

Background: Although major depressive disorder (MDD) represents one of the most serious psychiatric problems afflicting adolescents, efforts to understand the neural circuitry of adolescent MDD have lagged behind those of adult MDD. This study tests the hypothesis that adolescent MDD is associated with abnormal amygdala activity during evocative-face viewing. Methods: Using functional magnetic resonance imaging (fMRI), between-group differences among MDD (n = 10), anxious (n = 11), and non-psychiatric comparisons (n = 23) were examined during successful vs. unsuccessful face encoding, with encoding success measured post-scan. Results: Compared to healthy adolescents, MDD patients exhibited poorer memory for faces. fMRI analyses accounted for this performance difference through event-related methods. In an analysis comparing successful vs. unsuccessful face encoding, MDD patients exhibited greater left amygdala activation relative to healthy and anxious youth. Conclusions: Given prior findings among adults, this study suggests that adolescent and adult MDD may involve similar underlying abnormalities in amygdala functioning. [Copyright &y& Elsevier]

The COVID-19 pandemic generated significant life stress and increases in internalizing disorders. Moreover, COVID-related stressors disproportionately impacted women, consistent with outcomes showing a gender gap in stress-related disorders. Gender-related stress vulnerability emerges in adolescence alongside gender-specific changes in neuroendocrine signaling. Most research on the neuroendocrinology of stress-related disorders has focused on differences in the hypothalamic-pituitary-adrenal (HPA) axis effector hormone cortisol. More recent studies, however, emphasize dehydroepiandrosterone (DHEA), a neuroprotective and neuroactive hormone released concurrently with cortisol that balances its biobehavioral actions during stress. Notably, women show lower cortisol responses and higher DHEA responses to stress. However, lower cortisol and higher DHEA are associated with internalizing disorders in women, while those associations are opposite in men. Thus, gender-specific factors perhaps result in a neuroendocrine profile that places women at greater risk for stress-related disorders. The current study prospectively examined socially evaluated cold-pressor task (SECPT) induced neuroendocrine responses at age 15 and internalizing symptoms during the COVID-19 pandemic at age 21 in a cohort of 175 primarily Black low-socioeconomic status participants, while controlling for internalizing symptoms at age 15. The association between COVID-related stress and internalizing symptoms was not stronger in women. Lower DHEA-cortisol ratios were associated with a weaker relationship between COVID-related stress and internalizing symptoms in women, while higher ratios were associated with a weaker relationship in men. These findings suggest gender differences in the relationship between DHEA and cortisol and internalizing outcomes during a stressful period, and support differential neuroendocrine protective and risk pathways for young men and women. • DHEA-cortisol ratios moderated the COVID-related stress and internalizing symptoms association differently by gender. • COVID-related stress predicted fewer depression and anxiety symptoms for women with low and average DHEA-cortisol ratios. • COVID-related stress predicted fewer anxiety symptoms for men with high DHEA-cortisol ratios. • Our sample was 175 primarily Black low-SES young adults, who were likely to experience significant hardship during COVID. [ABSTRACT FROM AUTHOR]

Background Research suggests that individuals with anxiety have difficulty ignoring threat distractors when completing tasks with competing stimuli. Studies examining the neural correlates of these emotional processing difficulties in youth anxiety highlight reduced recruitment of regions associated with goal-directed attention, such as the anterior cingulate cortex (ACC). In the current study, we examined neural activation during an emotional conflict task in youth with anxiety disorders before and after treatment. Methods Twenty-five youth (ages 9–19 years) with generalized, separation, and/or social anxiety disorder and 25 healthy controls underwent 2 functional magnetic resonance imaging scans approximately 13 weeks apart. At each scan, participants completed a task in which they matched shapes in the context of emotional distractors (happy and threatening faces). Between scans, anxious youth were treated with the selective serotonin reuptake inhibitor (SSRI) sertraline or cognitive behavior therapy (CBT). Results Prior to treatment, anxious youth exhibited reduced activation of the medial prefrontal cortex, encompassing the rostral ACC, when matching shapes in the context of threat distractors relative to healthy controls. Activation in this region increased in anxious youth after treatment, but remained unchanged in the healthy control group. Increases in rostral ACC activation were related to greater reductions in social anxiety and avoidance symptoms following treatment. Conclusions Effective treatments for pediatric anxiety may enhance rostral ACC response during attempts to filter out threat-relevant stimuli. Enhanced recruitment of this region may constitute one manner in which CBT and SSRI treatment reduce youth anxiety symptoms, particularly social anxiety and avoidance. [ABSTRACT FROM AUTHOR]

Increased error monitoring, as measured by the error-related negativity (ERN), has been shown to persist after treatment for obsessive-compulsive disorder in youth and adults; however, no previous studies have examined the ERN following treatment for related anxiety disorders. We used a flanker task to elicit the ERN in 28 youth and young adults (8–26 years old) with primary diagnoses of generalized anxiety disorder (GAD) or social anxiety disorder (SAD) and 35 healthy controls. Patients were assessed before and after treatment with cognitive-behavioral therapy (CBT) or selective serotonin reuptake inhibitors (SSRI), and healthy controls were assessed at a comparable interval. The ERN increased across assessments in the combined sample. Patients with SAD exhibited an enhanced ERN relative to healthy controls prior to and following treatment, even when analyses were limited to SAD patients who responded to treatment. Patients with GAD did not significantly differ from healthy controls at either assessment. Results provide preliminary evidence that enhanced error monitoring persists following treatment for SAD in youth and young adults, and support conceptualizations of increased error monitoring as a trait-like vulnerability that may contribute to risk for recurrence and impaired functioning later in life. Future work is needed to further evaluate the ERN in GAD across development, including whether an enhanced ERN develops in adulthood or is most apparent when worries focus on internal sources of threat. [ABSTRACT FROM AUTHOR]

Threat-related amygdala reactivity and the activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis have been linked to negative psychiatric outcomes. The amygdala and HPA axis have bidirectional connections, suggesting that functional variation in one system may influence the other. However, research on the functional associations between these systems has demonstrated mixed findings, potentially due to small sample sizes and cortisol sampling and data analytic procedures that investigate only pre-post differences in cortisol rather than the specific phases of the cortisol stress response. Further, previous research has primarily utilized samples of adults of mostly European descent, limiting generalizability to those of other ethnoracial identities and ages. Therefore, studies addressing these limitations are needed in order to investigate the functional relations between amygdala reactivity to threat and HPA axis stress responsivity. Using a sample of 159 adolescents from a diverse cohort (75% African American, ages 15–17 years), the present study evaluated associations between amygdala reactivity during socioemotional processing using fMRI and HPA axis reactivity to a socially-evaluative cold pressor task. Greater amygdala activation to fearful and neutral faces was associated with greater cortisol peak values and steeper activation slope. As cortisol peak values and cortisol activation slope capture the intensity of the cortisol stress response, these data suggest that greater activation of the amygdala in response to social distress and ambiguity among adolescents may be related to hyper-reactivity of the HPA axis. • Greater amygdala activation to fear associated with greater cortisol activation slope. • We found coupling of amygdala and HPA axis activation to threat in separate tasks. • Our findings are based on a highly diverse sample of adolescents. [ABSTRACT FROM AUTHOR]

Functional neuroimaging studies have consistently demonstrated abnormalities in fear and threat processing systems in youth with anxiety disorders; however, the structural neuroanatomy of these systems in children and adolescents remains largely unknown. Using voxel-based morphometry (VBM), gray matter volumes were compared between 38 medication-free patients with anxiety disorders (generalized anxiety disorder; social phobia; separation anxiety disorder, mean age: 14.4 ± 3 years) and 27 comparison subjects (mean age: 14.8 ± 4 years). Compared to healthy subjects, youth with anxiety disorders had larger gray matter volumes in the dorsal anterior cingulate and had decreased gray matter volumes in the inferior frontal gyrus (ventrolateral prefrontal cortex), postcentral gyrus, and cuneus/precuneus. These data suggest the presence of structural differences in regions previously implicated in the processing and regulation of fear in pediatric patients with anxiety disorders. [ABSTRACT FROM AUTHOR]

Objective: Abnormalities of cognitive control functions, such as conflict and error monitoring, have been theorized to underlie obsessive-compulsive symptoms but only recently have been considered a potentially relevant psychological construct for understanding other forms of anxiety. The authors sought to determine whether these cognitive control processes elicit the same abnormalities of brain function in patients with pediatric obsessive-compulsive disorder (OCD) as in those with non-OCD anxiety disorders. Method: Functional magnetic resonance imaging of the Multisource Interference Task was used to measure conflict- and error-related activations in youth (8-18 years) with OCD (n = 21) and non-OCD anxiety disorders (generalized anxiety disorder, social phobia, separation anxiety disorder; n = 23) compared with age-matched healthy controls (n = 25). Results: There were no differences in performance (accuracy, response times) among groups. However, a significant effect of group was observed in the dorsolateral prefrontal cortex (dlPFC) during error processing, driven by decreased activation in patients with OCD and those with non-OCD anxiety compared with healthy youth. Between patient groups, there was no difference in error-related dlPFC activation. Conclusions: Hypoactive dlPFC response to errors occurs in pediatric patients with OCD and those with non-OCD anxiety. These findings suggest that insufficient error-related engagement of the dlPFC associates with anxiety across traditional diagnostic boundaries and appears during the early stages of illness. [ABSTRACT FROM AUTHOR]

• Adolescence is a critical period for reward processing development. • In adolescents, VS white matter connectivity is variable across the PFC. • VS–PFC white matter connectivity was related to VS functional activation to reward. • However, the relation between structure and activation varied by reward type. • The adolescent brain processes social and monetary rewards differently. The ventral striatum (VS) is implicated in reward processing and motivation. Human and non-human primate studies demonstrate that the VS and prefrontal cortex (PFC), which comprise the frontostriatal circuit, interact to influence motivated behavior. However, there is a lack of research that precisely maps and quantifies VS–PFC white matter tracts. Moreover, no studies have linked frontostriatal white matter to VS activation. Using a multimodal neuroimaging approach with diffusion MRI (dMRI) and functional MRI (fMRI), the present study had two objectives: 1) to chart white matter tracts between the VS and specific PFC structures and 2) assess the association between the degree of VS–PFC white matter tract connectivity and VS activation in 187 adolescents. White matter connectivity was assessed with probabilistic tractography and functional activation was examined with two fMRI tasks (one task with social reward and another task using monetary reward). We found widespread but variable white matter connectivity between the VS and areas of the PFC, with the anterior insula and subgenual cingulate cortex demonstrating the greatest degree of connectivity with the VS. VS–PFC structural connectivity was related to functional activation in the VS though activation depended on the specific PFC region and reward task. [ABSTRACT FROM AUTHOR]

The article presents a study on amygdala habituation, the decrease in responsiveness to repeated stimuli, to faces and its relationship to ventromedial prefrontal cortex (vmPFC)-amygdala connectivity among adolescents with autism spectrum disorders (ASD). Research involved using magnetic resonance imaging on ASD patients while they participated in a task involving identifying gender and emotion. Results indicated a strong correlation between autism severity and decreased amygdala habituation.

Abstract: Healthy individuals show robust functional connectivity during rest, which is stronger in adults than in children. Connectivity occurs between the posterior and anterior portions of the default network, a group of structures active in the absence of a task, including the posterior cingulate cortex and the superior frontal gyrus. Previous studies found weaker posterior–anterior connectivity in the default network in adults and adolescents with autism spectrum disorders (ASD). However, these studies used small a priori regions of interest (“seeds”) to calculate connectivity. Since seed location for all participants was chosen based on controls'' brains, these studies'' analyses are more tailored to controls than individuals with ASD. An alternative is to use a data-driven approach, such as self-organizing maps (SOM), to create a reference for each participant to calculate connectivity. We used individualized resting-state clusters identified by an SOM algorithm to corroborate previous findings of weaker posterior–anterior connectivity in the ASD group and examine age-related changes in the ASD and control groups. Thirty-nine adolescents with ASD and 41 controls underwent a 10-minute, eyes-open, resting-state functional MRI scan. The SOM analysis revealed that adolescents with ASD versus controls have weaker connectivity between the posterior hub of the default network and the right superior frontal gyrus. Additionally, controls have larger increases in connectivity with age compared to the ASD group. These findings indicate that SOM is a complementary method for calculating connectivity in a clinical population. Additionally, adolescents with ASD have a different developmental trajectory of the default network compared to controls. [Copyright &y& Elsevier]

Abstract: Autism spectrum disorders (ASD) are associated with disturbances of neural connectivity. Functional connectivity between neural structures is typically examined within the context of a cognitive task, but also exists in the absence of a task (i.e., “rest”). Connectivity during rest is particularly active in a set of structures called the default network, which includes the posterior cingulate cortex (PCC), retrosplenial cortex, lateral parietal cortex/angular gyrus, medial prefrontal cortex, superior frontal gyrus, temporal lobe, and parahippocampal gyrus. We previously reported that adults with ASD relative to controls show areas of stronger and weaker connectivity within the default network. The objective of the present study was to examine the default network in adolescents with ASD. Sixteen adolescents with ASD and 15 controls participated in a functional MRI study. Functional connectivity was examined between a PCC seed and other areas of the default network. Both groups showed connectivity in the default network. Relative to controls, adolescents with ASD showed widespread weaker connectivity in nine of the eleven areas of the default network. Moreover, an analysis of symptom severity indicated that poorer social skills and increases in restricted and repetitive behaviors and interests correlated with weaker connectivity, whereas poorer verbal and non-verbal communication correlated with stronger connectivity in multiple areas of the default network. These findings indicate that adolescents with ASD show weaker connectivity in the default network than previously reported in adults with ASD. The findings also show that weaker connectivity within the default network is associated with specific impairments in ASD. [Copyright &y& Elsevier]

Abstract: The ability of positive and negative facial signals to influence attention orienting is crucial to social functioning. Given the dramatic developmental change in neural architecture supporting social function, positive and negative facial cues may influence attention orienting differently in relatively young or old individuals. However, virtually no research examines such age-related differences in the neural circuitry supporting attention orienting to emotional faces. We examined age-related correlations in attention-orienting biases to positive and negative face emotions in a healthy sample (N =37; 9–40 years old) using functional magnetic resonance imaging and a dot-probe task. The dot-probe task in an fMRI setting yields both behavioral and neural indices of attention biases towards or away from an emotional cue (happy or angry face). In the full sample, angry-face attention bias scores did not correlate with age, and age did not correlate with brain activation to angry faces. However, age did positively correlate with attention bias towards happy faces; age also negatively correlated with left cuneus and left caudate activation to a happy bias fMRI contrast. Secondary analyses suggested age-related changes in attention bias to happy faces. The tendency in younger children to direct attention away from happy faces (relative to neutral faces) was diminished in the older age groups, in tandem with increasing neural deactivation. Implications for future work on developmental changes in attention–emotion processing are discussed. [Copyright &y& Elsevier]

Background: Associations between a functional polymorphism in the serotonin transporter gene and amygdala activation have been found in healthy, depressed, and anxious adults. This study explored these gene–brain associations in adolescents by examining predictive effects of serotonin transporter gene variants (S and LG allele carriers vs. LA allele homozygotes) and their interaction with diagnosis (healthy vs. patients) on amygdala responses to emotional faces. Methods: Functional magnetic resonance data were collected from 33 healthy adolescents (mean age: 13.71, 55% female) and 31 medication-free adolescents with current anxiety or depressive disorders (or both; mean age: 13.58, 56% female) while viewing fearful, angry, happy, and neutral facial expressions under varying attention states. Results: A significant three-way genotype-by-diagnosis-by-face-emotion interaction characterized right amygdala activity while subjects monitored internal fear levels. This interaction was decomposed to map differential gene–brain associations in healthy and affected adolescents. First, consistent with healthy adult data, healthy adolescents with at least one copy of the S or LG allele showed stronger amygdala responses to fearful faces than healthy adolescents without these alleles. Second, patients with two copies of the LA allele exhibited greater amygdala responses to fearful faces relative to patients with S or LG alleles. Third, although weaker, genotype differences on amygdala responses in patients extended to happy faces. All effects were restricted to the fear-monitoring attention state. Conclusions: S/LG alleles in healthy adolescents, as in healthy adults, predict enhanced amygdala activation to fearful faces. Contrary findings of increased activation in patients with LALA relative to the S or LG alleles require further exploration. [Copyright &y& Elsevier]

Abstract: Using event-related functional magnetic resonance imaging (fMRI) with a visual-probe task that assesses attention to threat, we investigated the cognitive and neurophysiological correlates of trait anxiety in youth. During fMRI acquisition, 16 healthy children and adolescents viewed angry-neutral face pairs and responded to a probe that was on the same (angry-congruent) or opposite (angry-incongruent) side as the angry face. Attention bias scores were calculated by subtracting participants’ mean reaction time for angry-congruent trials from angry-incongruent trials. Trait anxiety was positively associated with attention bias towards angry faces. Neurophysiologically, trait anxiety was positively associated with right dorsolateral prefrontal cortex (PFC) activation on a contrast of trials that reflect the attention bias for angry faces (i.e. angry-incongruent versus angry-congruent trials). Trait anxiety was also positively associated with right ventrolateral PFC activation on trials with face stimuli (vesus baseline), irrespective of their emotional content. [Copyright &y& Elsevier]

Objective: The purpose of this study is to examine processing of facial emotions in a sample of maltreated children showing high rates of post-traumatic stress disorder (PTSD). Maltreatment during childhood has been associated independently with both atypical processing of emotion and the development of PTSD. However, research has provided little evidence indicating how high rates of PTSD might relate to maltreated children''s processing of emotions. Method: Participants’ reaction time and labeling of emotions were measured using a morphed facial emotion identification task. Participants included a diverse sample of maltreated children with and without PTSD and controls ranging in age from 8 to 15 years. Maltreated children had been removed from their homes and placed in state custody following experiences of maltreatment. Diagnoses of PTSD and other disorders were determined through combination of parent, child, and teacher reports. Results: Maltreated children displayed faster reaction times than controls when labeling emotional facial expressions, and this result was most pronounced for fearful faces. Relative to children who were not maltreated, maltreated children both with and without PTSD showed enhanced response times when identifying fearful faces. There was no group difference in labeling of emotions when identifying different facial emotions. Conclusions: Maltreated children show heightened ability to identify fearful faces, evidenced by faster reaction times relative to controls. This association between maltreatment and atypical processing of emotion is independent of PTSD diagnosis. [Copyright &y& Elsevier]

We examined neural activations during decision-making using fMRI paired with the wheel of fortune task, a newly developed two-choice decision-making task with probabilistic monetary gains. In particular, we assessed the impact of high-reward/risk events relative to low-reward/risk events on neural activations during choice selection and during reward anticipation. Seventeen healthy adults completed the study. We found, in line with predictions, that (i) the selection phase predominantly recruited regions involved in visuo-spatial attention (occipito-parietal pathway), conflict (anterior cingulate), manipulation of quantities (parietal cortex), and preparation for action (premotor area), whereas the anticipation phase prominently recruited regions engaged in reward processes (ventral striatum); and (ii) high-reward/risk conditions relative to low-reward/risk conditions were associated with a greater neural response in ventral striatum during selection, though not during anticipation. Following an a priori ROI analysis focused on orbitofrontal cortex, we observed orbitofrontal cortex activation (BA 11 and 47) during selection (particularly to high-risk/reward options), and to a more limited degree, during anticipation. These findings support the notion that (1) distinct, although overlapping, pathways subserve the processes of selection and anticipation in a two-choice task of probabilistic monetary reward; (2) taking a risk and awaiting the consequence of a risky decision seem to affect neural activity differently in selection and anticipation; and thus (3) common structures, including the ventral striatum, are modulated differently by risk/reward during selection and anticipation. [Copyright &y& Elsevier]

Background: Although comorbid anxiety disorders are common in children with bipolar disorder (BD), it is unclear how this comorbidity impacts the pathophysiology of the illness. Methods: Pediatric BD with lifetime anxiety (BD+ANX, n = 20), BD without lifetime anxiety (BD-ANX, n = 11), and controls (n = 14) were administered the visual-probe paradigm, which assesses attention bias to threat faces. Results: Bipolar disorder +ANX demonstrated a stronger bias toward threat relative to BD-ANX and controls; the latter two did not differ from each other. Conclusions: Bipolar disorder +ANX showed a bias toward threat while, in two previous studies, anxious children showed a bias away from threat faces. Future studies should compare the pathophysiology of BD with and without a comorbid anxiety disorder and anxiety disorders presenting alone. [Copyright &y& Elsevier]

• Different dimensions of childhood adversity are important for HPA-axis function. • Childhood violence exposure predicted a blunted cortisol response in adolescence. • Childhood social deprivation was not associated with adolescents' cortisol response. • The effect of violence exposure on peak activation was moderated by social deprivation. The present study tested how two different dimensions of childhood adversity, violence exposure and social deprivation, were associated with the cortisol response to the Socially Evaluated Cold-Pressor task in a sample of 222 adolescents (n = 117 girls, n = 167 African American). Participants were part of the Fragile Families and Child Wellbeing Study, a probability sample of births in large US cities (>200,000) between 1998 and 2000. Our subsample includes births in three cities: Detroit, Toledo, and Chicago. The study design called for an oversampling of births to unmarried parents (3:1) which led to a large number of minority and economically disadvantaged adolescents. When children were ages 3, 5, and 9, mothers reported on exposures to violence and social deprivation that occurred in the past year. Exposures from the three waves were averaged to reflect violence exposure and social deprivation during childhood. Greater levels of violence exposure from ages 3 to 9 were associated with a blunted cortisol response to stress at age 15, even after controlling for social deprivation and other factors known to influence cortisol reactivity. Social deprivation from ages 3 to 9 was not associated with the cortisol response to stress; though in an exploratory analysis, social deprivation moderated the association between violence exposure and cortisol peak activation. In line with the Dimensional Model of Adversity and Psychopathology, these findings suggest that experiences of violence, but not social deprivation, during childhood may contribute to cortisol blunting that has been previously reported in samples with high levels of social deprivation. Findings from the present longitudinal study on a relatively large sample of under-represented minority youth provide insight into the ways two different dimensions of childhood adversity impact the cortisol response to stress. [ABSTRACT FROM AUTHOR]