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Rumination is a significant risk factor for psychopathology in adolescent girls and is associated with heightened and prolonged physiological arousal following social rejection. However, no study has examined how rumination relates to neural responses to social rejection in adolescent girls; thus, the current study aimed to address this gap. Adolescent girls (N = 116; ages 16.95-19.09) self-reported on their rumination tendency and completed a social evaluation fMRI task where they received fictitious feedback (acceptance, rejection) from peers they liked or disliked. Rejection-related neural activity and subgenual anterior cingulate cortex (sgACC) connectivity were regressed on rumination, controlling for rejection sensitivity and depressive symptoms. Rumination was associated with distinctive neural responses following rejection from liked peers including increased neural activity in the precuneus, inferior parietal gyrus, dorsolateral prefrontal cortex, and supplementary motor area (SMA) and reduced sgACC connectivity with multiple regions including medial prefrontal cortex, precuneus and ventrolateral prefrontal cortex. Greater precuneus and SMA activity mediated the effect of rumination on slower response time to report emotional state after receiving rejection from liked peers. These findings provide clues for distinctive cognitive processes (e.g., mentalizing, conflict processing, memory encoding) following the receipt of rejection in girls with high levels of rumination.

The Environmental Influences on Child Health Outcomes (ECHO)-Wide Cohort Study (EWC), a collaborative research design comprising 69 cohorts in 31 consortia, was funded by the National Institutes of Health (NIH) in 2016 to improve children's health in the United States. The EWC harmonizes extant data and collects new data using a standardized protocol, the ECHO-Wide Cohort Data Collection Protocol (EWCP). EWCP visits occur at least once per life stage, but the frequency and timing of the visits vary across cohorts. As of March 4, 2022, the EWC cohorts contributed data from 60,553 children and consented 29,622 children for new EWCP data and biospecimen collection. The median (interquartile range) age of EWCP-enrolled children was 7.5 years (3.7-11.1). Surveys, interviews, standardized examinations, laboratory analyses, and medical record abstraction are used to obtain information in 5 main outcome areas: pre-, peri-, and postnatal outcomes; neurodevelopment; obesity; airways; and positive health. Exposures include factors at the level of place (e.g., air pollution, neighborhood socioeconomic status), family (e.g., parental mental health), and individuals (e.g., diet, genomics).

Regulation of negative emotions is a core competency of child development. Parental emotion socialization profoundly influences later capacity to regulate negative affect in childhood and adolescence. The present study examined the effects of maternal emotion socialization on the development of emotion regulation in the context of a longitudinal study of 210 mother-daughter dyads. Dyads completed a conflict resolution task when the child was age 11 years during which maternal warmth and hostility were coded. At ages 11 to 13 years, mothers completed self-report measures of supportive and nonsupportive responses to child negative emotion, and children completed self-reports of inhibition and adaptive regulation of sadness and anger. We used latent growth curve modeling to estimate changes in inhibition and adaptive regulation of sadness and anger over time; observed maternal warmth and hostility were included as time-invariant covariates and maternal self-report of supportive and nonsupportive responses were included as time-varying covariates. Observed maternal warmth was positively associated with girls adaptive regulation of anger and sadness at age 11 years. Maternal self-reported supportive responses to girls negative affect were positively associated with girls adaptive regulation of anger, and nonsupportive responses were negatively associated with adaptive regulation of anger and sadness. These findings support the role of maternal emotion socialization and indicate specific effects of maternal warmth and supportive responses in the development of girls capacity to modulate negative emotions during early adolescence. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Anhedonia is a transdiagnostic symptom of psychopathology that includes diminished positive emotions and anticipation and enjoyment of reward, with particular salience during adolescence. However, the construct validity of anhedonia dimensions is not well established, thus limiting operationalization and generalization of the construct. We applied exploratory and confirmatory factor analyses to identify latent dimensions of anhedonia across four commonly used self-report measures covering different facets of anhedonic experience within a nonclinical sample of female adolescents across two waves of data collection (N = 173, Mage = 19.25; N = 147, Mage = 20.23). Factor analyses yielded a two-factor model with a physical anhedonia factor emphasizing enjoyment from physical sensations and a social anhedonia factor focusing on emotional connections with other people. These results have implications for the measurement of anhedonia in women's emotional well-being and mental health research, including research designed to identify facets of anhedonia that predict the onset, severity, and persistence of psychopathology. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Negative emotional experiences can be more difficult to forget than neutral ones, a phenomenon termed the "emotional memory effect." Individual differences in the strength of the emotional memory effect are associated with emotional health. Thus, understanding the neurobiological underpinnings of the emotional memory effect has important implications, especially for individuals at risk for emotional health problems. Although the neural basis of emotional memory effects has been relatively well defined, less is known about how hormonal factors that can modulate emotional memory, such as glucocorticoids, relate to that neural basis. Importantly, probing the role of glucocorticoids in the stress- and emotion-sensitive period of late childhood to adolescence could provide actionable points of intervention. We addressed this gap by testing whether hypothalamic-pituitary-adrenal (HPA) axis activity during a parent-child conflict task at 11 years of age predicted emotional memory and its primary neural circuitry (i.e., amygdala-hippocampus functional connectivity) at 16 years of age in a longitudinal study of 147 girls (104 with complete data). Results showed that lower HPA axis activity predicted stronger emotional memory effects, r(124) = -.236, p < .01, and higher emotional memory-related functional connectivity between the right hippocampus and the right amygdala, β = -.385, p < .001. These findings suggest that late childhood HPA axis activity may modulate the neural circuitry of emotional memory effects in adolescence, which may confer a potential risk trajectory for emotional health among girls.

BackgroundGirls' depressive symptoms typically increase in adolescence, with individual differences in course and severity being key risk factors for impaired emotional functioning in young adulthood. Given the continued brain white matter (WM) maturation that occurs in adolescence, the present study tested whether structural connectivity patterns in late adolescence are associated with variation in the course of depression symptom severity throughout adolescence.MethodParticipants were girls (N = 115) enrolled in a multiyear prospective cohort study of risk for depression. Initial depression severity (intercept) at age 10 and change in severity (linear slope) across ages 10-19 were examined in relation to WM tractography collected at age 19. Network-based statistic analyses were used to identify clusters showing variation in structural connectivity in association with depressive symptom intercept, slope, and their interaction.ResultsHigher initial depressive severity and steeper positive slope (separately) were associated with greater structural connectivity between temporal, subcortical socioaffective, and occipital regions. Intercept showed more connectivity associations than slope. The interaction effect indicated that higher initial symptom severity and a steeper negative slope (i.e., alleviating symptoms) were related to greater connectivity between cognitive control regions. Moderately severe symptoms that worsened over time were followed by greater connectivity between self-referential and cognitive regions (e.g., posterior cingulate and frontal gyrus).ConclusionsHigher depressive symptom severity in early adolescence and increasing symptom severity over time may forecast structural connectivity differences in late adolescence, particularly in pathways involving cognitive and emotion-processing regions. Understanding how clinical course relates to neurobiological correlates may inform new treatment approaches to adolescent depression.

Functional neuroimaging results need to replicate to inform sound models of human social cognition and its neural correlates. Introspection, the capacity to reflect on one's thoughts and feelings, is one process required for normative social cognition and emotional functioning. Engaging in introspection draws on a network of brain regions including medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), middle temporal gyri (MTG), and temporoparietal junction (TPJ). Maturation of these regions during adolescence mirrors the behavioral advances seen in adolescent social cognition, but the neural correlates of introspection in adolescence need to replicate to confirm their generalizability and role as a possible mechanism. The current study investigated whether reflecting upon one's own feelings of sadness would activate and replicate similar brain regions in two independent samples of adolescents. Participants included 156 adolescents (50% female) from the California Families Project and 119 adolescent girls from the Pittsburgh Girls Study of Emotion. All participants completed the Emotion Regulation Questionnaire (ERQ) and underwent a functional magnetic resonance imaging scan while completing the same facial emotion-processing task at age 16-17 years. Both samples showed similar whole-brain activation patterns when engaged in sadness introspection and when judging a nonemotional facial feature. Whole-brain activation was unrelated to ERQ scores in both samples. Neural responsivity to task manipulations replicated in regions recruited for socio-emotional (mPFC, PCC, MTG, TPJ) and attention (dorsolateral PFC, precentral gyri, superior occipital gyrus, superior parietal lobule) processing. These findings demonstrate robust replication of neural engagement during sadness introspection in two independent adolescent samples.

Patterns of pubertal maturation have been linked to vulnerability for emotion dysregulation disorders in girls, as well as white matter (WM) development, suggestive of a potential mechanism between pubertal maturation and emotional health. Because pubertal processes begin at varying ages (i.e., status, timing) and proceed at varying rates (i.e., tempo), identifying individual differences in the pubertal course associated with subsequent WM microstructure development may reveal clues about neurobiological mechanisms of girls' emotional well-being. In a prospective cohort study of 107 girls, we examined associations between pubertal status at age 9, pubertal timing and tempo from ages 9-15, and WM microstructure at age 19. Tract-based spatial statistics revealed that girls with more advanced pubertal status at age 9, specific to gonadal-related physical changes, had higher fractional anisotropy, and lower mean diffusivity (MD) and radial diffusivity in tracts relevant to cognitive control and emotion regulation (e.g., the superior longitudinal fasciculus, external capsule, and uncinate fasciculus). Additionally, girls with earlier pubertal timing showed lower MD in the left anterior cingulum bundle. Tempo was unrelated to WM measures. These findings implicate specific aspects of pubertal maturation in subsequent neural signatures, suggesting possible neuroendocrine mechanisms relevant to emotional development. Future work incorporating longitudinal neuroimaging in parallel with pubertal measures may contribute to the understanding of individual variation in pubertal course and WM development.

The present study used cross-lagged panel analyses to test longitudinal associations among emotion regulation, prefrontal cortex (PFC) function, and depression severity in adolescent girls. The ventromedial and dorsomedial PFC (vmPFC and dmPFC) were regions of interest given their roles in depression pathophysiology, self-referential processing, and emotion regulation. At ages 16 and 17, seventy-eight girls completed a neuroimaging scan to assess changes in vmPFC and dmPFC activation to sad faces, and measures of depressive symptom severity and emotion regulation. The 1-year cross-lagged effects of dmPFC activity at age 16 on expressive suppression at age 17 and depressive symptomatology at age 17 were significant, demonstrating a predictive relation between dmPFC activity and both suppression and depressive severity.

PURPOSE:Neuroimaging studies suggest that altered brain responses to food-related cues in reward-sensitive regions characterize individuals who experience binge-eating episodes. However, the absence of longitudinal data limits the understanding of whether reward-system alterations increase vulnerability to binge eating, as theorized in models of the development of this behavior. METHODS:Adolescent girls (N = 122) completed a functional magnetic resonance imaging monetary reward task at age 16 years as part of an ongoing longitudinal study. Self-report of binge eating was assessed using the Eating Attitudes Test at ages 16 and 18 years. Regression analyses examined concurrent and longitudinal associations between the blood-oxygenation-level-dependent response to anticipating and winning monetary rewards and the severity of binge eating while controlling for age 16 depressive symptoms and socioeconomic status. RESULTS:Greater ventromedial prefrontal cortex and caudate responses to winning money were correlated with greater severity of binge eating concurrently but not prospectively. CONCLUSIONS:This study is the first to examine longitudinal associations between reward responding and binge eating in community-based, mostly low-socioeconomic status adolescent girls. Ventromedial prefrontal cortex response to reward outcome-possibly reflecting an enhanced subjective reward value-appears to be a state marker of binge-eating severity rather than a predictor of future severity.

ObjectiveGiven the association between maternal caregiving behavior and heightened neural reward activity in experimental animal studies, the present study examined whether motherhood in humans positively modulates reward-processing neural circuits, even among mothers exposed to various life stressors and depression.MethodsSubjects were 77 first-time mothers and 126 nulliparous young women from the Pittsburgh Girls Study, a longitudinal study beginning in childhood. Subjects underwent a monetary reward task during functional magnetic resonance imaging in addition to assessment of current depressive symptoms. Life stress was measured by averaging data collected between ages 8-15 years. Using a region-of-interest approach, we conducted hierarchical regression to examine the relationship of psychosocial factors (life stress and current depression) and motherhood with extracted ventral striatal (VST) response to reward anticipation. Whole-brain regression analyses were performed post-hoc to explore non-striatal regions associated with reward anticipation in mothers vs nulliparous women.ResultsAnticipation of monetary reward was associated with increased neural activity in expected regions including caudate, orbitofrontal, occipital, superior and middle frontal cortices. There was no main effect of motherhood nor motherhood-by-psychosocial factor interaction effect on VST response during reward anticipation. Depressive symptoms were associated with increased VST activity across the entire sample. In exploratory whole brain analysis, motherhood was associated with increased somatosensory cortex activity to reward (FWE cluster forming threshold p

Study objectivesEmerging evidence suggests that insomnia may disrupt reward-related brain function-a potentially important factor in the development of depressive disorder. Adolescence may be a period during which such disruption is especially problematic given the rise in the incidence of insomnia and ongoing development of neural systems that support reward processing. The present study uses longitudinal data to test the hypothesis that disruption of neural reward processing is a mechanism by which insomnia symptoms-including nocturnal insomnia symptoms (NIS) and nonrestorative sleep (NRS)-contribute to depressive symptoms in adolescent girls.MethodParticipants were 123 adolescent girls and their caregivers from an ongoing longitudinal study of precursors to depression across adolescent development. NIS and NRS were assessed annually from ages 9 to 13 years. Girls completed a monetary reward task during a functional MRI scan at age 16 years. Depressive symptoms were assessed at ages 16 and 17 years. Multivariable regression tested the prospective associations between NIS and NRS, neural response during reward anticipation, and the mean number of depressive symptoms (omitting sleep problems).ResultsNRS, but not NIS, during early adolescence was positively associated with late adolescent dorsal medial prefrontal cortex (dmPFC) response to reward anticipation and depressive symptoms. DMPFC response mediated the relationship between early adolescent NRS and late adolescent depressive symptoms.ConclusionsThese results suggest that NRS may contribute to depression by disrupting reward processing via altered activity in a region of prefrontal cortex involved in affective control. The results also support the mechanistic differentiation of NIS and NRS.

BackgroundChildren who experience socioeconomic disadvantage are at heightened risk for developing depression; however, little is known about neurobiological mechanisms underlying this association. Low socioeconomic status (SES) during childhood may confer risk for depression through its stress-related effects on the neural circuitry associated with processing monetary rewards.MethodsIn a prospective study, we examined the relationships among the number of years of household receipt of public assistance from age 5-16 years, neural activation during monetary reward anticipation and receipt at age 16, and depression symptoms at age 16 in 123 girls.ResultsNumber of years of household receipt of public assistance was positively associated with heightened response in the medial prefrontal cortex during reward anticipation, and this heightened neural response mediated the relationship between socioeconomic disadvantage and current depression symptoms, controlling for past depression.ConclusionsChronic exposure to socioeconomic disadvantage in childhood may alter neural circuitry involved in reward anticipation in adolescence, which in turn may confer risk for depression.