Journal of Child Psychology and Psychiatry

ObjectiveChildhood poverty is a high-risk context that involves diverse adversities, making it difficult to understand how poverty confers later psychopathology risk and why some children remain resilient despite growing up in poverty. To address this heterogeneity, we quantified adversity-linked vulnerability as adversity-psychopathology coupling and tested whether childhood poverty amplifies this coupling and whether multilevel inhibitory-control profiles stratify vulnerability and resilience within poverty-exposed youth. MethodsWe analyzed 10,112 youth (48.4% female; mean age = 9.92 years) from the Adolescent Brain Cognitive Development Study, linking baseline cumulative early-life adversity (ELA) to later behavioral problems across 4 waves. In the stop-signal task fMRI subsample of 7,401 youth, semi-supervised clustering of inhibitory-control activation identified neurofunctional subtypes within poverty-exposed youth. We also tested temperamental inhibitory control as an additional moderator. ResultsChildhood poverty amplified the association between cumulative ELA and behavioral problems at baseline ({Delta}{beta} = 0.088; P < .001) and across follow-up waves. Two neurofunctional subtypes were identified within poverty-exposed youth: subtype-1 showed greater vulnerability than higher-income peers ({Delta}{beta} = 0.149; P < .001), whereas subtype-2 showed attenuated vulnerability and did not differ from higher-income peers ({Delta}{beta} = 0.049; P = .135); this pattern persisted longitudinally. Among poverty-exposed youth in subtype-2 with high temperamental inhibitory control, the association between cumulative ELA and later behavioral problems was no longer significant. ConclusionsChildhood poverty strengthened the translation of adversity burden into later behavioral problems, but inhibitory-control profiles differentiated higher- and lower-risk pathways within poverty, highlighting inhibitory control as a candidate target for prevention.

Atypical social functioning is a core feature of autism, yet findings remain fragmented across components and development. We aimed to systematically integrate this literature and characterize the organization, development, and moderators of social functioning in autism. We conducted a systematic review and meta-analysis of behavioral studies published between January 1990 and August 2025, identified through PubMed, Web of Science, and prior reviews, including studies with clinically diagnosed autistic individuals and neurotypical controls. A qualitative synthesis and two complementary quantitative meta-analyses were performed, with risk of bias evaluated through study-level characteristics. A total of 2,622 studies (94,114 autistic and 172,847 neurotypical individuals across 32 countries) were included, covering 22 social components that clustered into five domains. Overall group differences were substantial (Hedges g = -0.744, 95% CI [-0.797, -0.690]). Differences emerged earliest in motivation-based processes ([~]6 months), followed by motor, emotion, and inference domains, and showed age-related divergence alongside improvement in some skills. Cross-domain analyses revealed stronger interdependencies in autism and an organizational pattern most consistent with serial relationships among domains. These findings should be interpreted in light of methodological heterogeneity, underpowered samples, and uneven cultural representation. Together, the results provide an integrative framework for understanding the organization and development of social functioning in autism, with implications for precision subtyping, developmentally timed interventions, and neurodiversity-informed research and policy. This study was pre-registered (PROSPERO: CRD42024566141).

BackgroundAttention-deficit/hyperactivity disorder (ADHD) has traditionally been conceptualized categorically, with efforts to identify disorder-specific neurobiological endophenotypes. However, dimensional models suggest that brain-behavior organization may follow developmental axes that cut across diagnostic boundaries. We tested whether neural dynamics and cortical excitability differentiate those with ADHD diagnoses from typically developing (TD) peers, and whether brain-behavior covariance aligns with diagnostic or developmental dimensions. MethodsWe studied 84 participants aged 8-17 years (51 ADHD, 33 TD). High-density electrophysiological (hdEEG) measures included task-free source-resolved data used to derive mean global brain fluidity (variance of dynamic functional connectivity) and region-specific cortical excitability. Behavioural measures included self- and parent-report questionnaires, cognitive control (CC) tasks, and neuropsychological tests. Partial least squares (PLS) assessed multivariate brain-behavior associations including age, followed by clustering based on latent component scores. ResultsGroup differences emerged in parent-report questionnaires and CC tasks, but not in neuropsychological measures. ADHD individuals showed higher mean global brain fluidity and increased cortical excitability. The excitability-fluidity relationship was network-dependent: higher excitability predicted higher fluidity in task-positive networks and lower fluidity in default-mode and salience networks, with no group effects. PLS identified a latent dimension linking neural metrics with age, verbal fluency, inhibitory control, and positive affect, but it did not distinguish ADHD from TD. Clustering revealed two neurodevelopmental profiles spanning both groups. ConclusionsWhile ADHD is associated with mean-level differences in neural dynamics, brain-behaviour organization follows a developmental neurocognitive-affective axis that transcends the diagnostic boundary. These findings support a dimensional framework for understanding neurobiological variation in neurodevelopmental conditions.

Objective: While ADHD symptoms often decline from childhood into adulthood, the underlying neurobiological mechanisms, such as altered brain maturation or neural reorganization, remain incompletely understood. This study investigated how grey matter development relates to ADHD symptom trajectories into adulthood. Method: We analyzed data of individuals with ADHD and controls from the longitudinal Dutch NeuroIMAGE cohort, utilizing dimensional ADHD symptom scores (Conners Parent Rating Scale) from three waves and T1-weighted structural MRI scans from the final two waves. Using General Linear Models with permutation-based inference, we examined: 1) cross-sectional associations between ADHD symptoms and vertex-wise cortical thickness and surface area, and subcortical volumes at Wave 1 (n = 765, mean age = 16.95 years); and 2) longitudinal associations between symptom progression and brain morphometric changes (Wave 0 to 1: n = 644, mean age = 11.55-17.24 years; Wave 1 to 2: n = 149, mean age = 16.45-20.11 years). Results: Cross-sectionally, at Wave 1, more ADHD symptoms were related to widespread reductions in surface area, most prominently in the frontal cortex, and smaller volumes of the cerebellum, amygdala, and hippocampus. Longitudinally, symptom improvement from Wave 1 to Wave 2 was associated with stronger reductions in surface area, particularly in prefrontal and occipital regions, and with more pronounced cortical thinning across multiple brain regions. Conclusion: These findings suggest an association between symptom trajectories and structural brain changes, indicating that clinical improvement in ADHD behaviors might coincide with ongoing neural refinement during the transition to adulthood.

BackgroundScreen use is pervasive in childhood and adolescence, yet its role in antisocial behaviour (ASB) remains uncertain. While cross-sectional studies consistently link higher screen use to elevated ASB, longitudinal evidence is mixed, and few studies have controlled adequately for prior behaviour and genetic liability. Thus, it remains unclear whether these associations reflect prospective influences of screen exposure, or underlying vulnerabilities shared with ASB. We investigated whether screen use is a modifiable risk factor or a marker of underlying vulnerability. MethodsWe analysed data from up to 41,562 children in the Norwegian Mother, Father, and Child Cohort Study (MoBa). ASB traits and ICD-10-based conduct disorder (CD) diagnoses were assessed at ages 5, 8 and 14 years, together with screen use (total exposure and modality). Cross-sectional logistic regression models examined associations between screen use and ASB traits/CD at each age, adjusting for sex and parental education. Polygenic risk scores for ASB (PRSASB) were used to assess genetic susceptibility and gene-environment interplay. Lagged logistic models tested whether screen use predicted later ASB, adjusting for prior ASB. Linear mixed-effects models examined developmental patterns across age. ResultsHigher screen use was positively associated with ASB traits and CD across all ages, with dose-response patterns across screen-use modalities. Social media showed the strongest modality-specific association at adolescence. In lagged models, screen use did not predict later ASB after adjustment for prior ASB. Longitudinal models showed significant but attenuating associations across development. PRSASB was independently and additively associated with ASB outcomes but did not interact with screen use. ConclusionsWe found that higher screen use was consistently associated with antisocial outcomes across childhood and adolescence. However, the absence of prospective associations after accounting for prior behaviour, together with independent genetic contributions, suggests that screen use may be better understood as a marker of underlying vulnerability rather than an independent driver of antisocial development.

Background: Adverse childhood experiences (ACEs) are traumatic or adverse events in early life that can have lasting effects on behavioral, emotional, and psychological functioning. Prior research suggests ACEs relate to later psychiatric outcomes through threshold, cumulative, and individual-specific risk patterns. Few studies, however, have operationalized all three models to test ACE-specific associations with diagnosed psychiatric disorders in individuals who are adopted or with foster care histories. Methods: We conducted a cross-sectional retrospective study using electronic health record data from foster care and adopted patients aged 0-21 years old seen at the University of Minnesota Adoption Medicine Clinic (UMN-AMC) between 2014-2024. Extracted measures included ACE history, demographics, and psychiatric diagnoses. We used latent class analysis and logistic regression to identify clusters of adversity and estimate associations with psychiatric diagnosis domains, adjusting for Sex and Age at Initial Visit. Results: ACEs showed a threshold pattern across psychiatric domains, with higher ACE counts associated with greater odds of psychiatric diagnoses. Individual risk modeling indicated that exposure to abuse or violence was associated with higher odds of psychiatric diagnoses. Across cumulative and individual risk approaches, Anxiety Disorders, Mood Disorders, and Behavioral or Emotional Disorders showed the greatest sensitivity to adversity. Conclusion: Current ACE models may not fully capture neurodevelopmental impacts reflected in diagnosed psychiatric disorders among adolescents, particularly in high-risk groups such as foster and adopted individuals. In a large clinic sample our findings support a nuanced association between ACEs and later psychiatric diagnoses and highlight the need for ACE-focused assessment, prevention, and treatment strategies tailored to foster care and adopted populations.

Understanding depressive symptoms dynamics and their determinants is crucial for designing effective mental health support initiatives. This study compared two methods for describing youth depressive symptoms trajectories and investigated associations of early-life factors (maternal education, maternal perinatal depression, domestic violence, physical, emotional, or sexual abuse, bullying victimisation, psychiatric disorder) with trajectory features. Prospective data from 8,264 mostly White European participants (54% female), including self-reported Short Moods and Feelings Questionnaires on ten occasions between 10-25 years, were used. Trajectories were summarised using functional principal component analysis (FPCA) and P-splines linear mixed-effect (PLME) models. Estimated derivatives were used to obtain magnitude and age of peak symptoms and peak symptoms velocity. Both methods performed comparably, but PLME models tended to over-smooth trajectories. Peak symptoms and peak velocity were higher and occurred >1 year earlier in females than males. All early-life factors were associated with higher peak symptoms, and most associated with higher and earlier peak velocity. Abuse and bullying additionally associated with earlier age of peak symptoms. FPCA is a useful alternative for characterising depressive symptoms trajectories and informing time-sensitive preventative measures to reduce impact of depression before symptoms reach their peak. Early-life stressors may accelerate timeline and intensity of symptoms escalation during adolescence. Lay summaryUnderstanding development of depressive symptoms and factors shaping them is crucial for designing effective mental health support initiatives. This study used data from over 8,000 young people regularly followed up from before birth to compare two cutting-edge methods for describing depressive symptoms trajectories and examined how known risk factors for adulthood depression relate to the severity and rate of change of depressive symptoms in adolescence. We found that both methods performed well and that the peaks in depressive symptoms and their rate of change were, on average, higher and occurred over a year earlier in females than males. Our findings additionally suggest that early-life stressors (e.g., abuse, bullying) may accelerate the development of depression, highlighting the importance of early prevention.

Objective: ADHD has been associated with obesity indicators, including BMI, across the lifespan. A possible mechanism linking ADHD and BMI is binge eating. Previous research has found associations between ADHD, binge eating and BMI. However, the role of genetic and environmental influences on these associations remains unclear. Method: We utilized data from the Twins Early Development Study (TEDS), comprising 3,675 monozygotic and 7,063 dizygotic twin pairs. ADHD symptoms in childhood and adolescence were assessed using parent-reported questionnaires. Adult ADHD symptoms were measured using both self-report and parent-report questionnaires. Phenotypic mediation models examined whether binge eating mediated the association between ADHD and BMI, without controlling for genetic confounding. Subsequently, the etiological architecture underlying the associations among the three traits across childhood, adolescence, and adulthood were investigated by incorporating genetic and environmental influences into the models. Results: Binge eating significantly mediated the association between ADHD symptoms and BMI in both adolescence and adulthood. However, these mediation effects were no longer present once genetic and environmental influences were incorporated into the models. The best-fitting model in childhood, adolescence and adulthood was Cholesky decomposition models, where covariance between traits was explained by shared aetiology. Conclusions: This twin study reveals shared liability across ADHD, binge eating, and BMI. The mediating role of binge eating in the relationship between ADHD symptoms and BMI was largely confounded by shared genetic influences. Intervention strategies could focus more on common underlying behavioural and self-regulatory mechanisms across these traits, as well as placing more emphasis on symptom patterns within families.

Mind wandering has been linked to a wide range of psychiatric conditions, yet most studies have examined these associations in isolation. Given the substantial comorbidity across the psychopathological spectrum, it remains unclear whether elevated mind wandering reflects a general marker of psychopathology or a more specific attentional-control deficit shared across symptom dimensions. To address this, we adopted a dimensional, transdiagnostic approach in a non-clinical sample (N = 376), simultaneously modeling seven symptom dimensions: ADHD, depression, obsessive-compulsive tendencies, schizotypy, autistic traits, hypomania, and eating disorder symptoms. At the bivariate level, mind wandering correlated positively with all symptom dimensions. However, when the substantial shared variance across dimensions was accounted for in both frequentist and Bayesian multivariate regression models, only ADHD symptoms emerged as a unique predictor ({beta} = 0.53; BF{square}{square} > 1000), with all remaining predictors yielding negligible unique contributions and Bayes factors supporting the null hypothesis. These findings suggest that previously reported associations between mind wandering and diverse psychopathological symptom dimensions largely reflect a shared liability with ADHD-related attentional dysregulation, rather than disorder-specific mechanisms. This positions mind wandering as a marker of attentional dysregulation more closely tied to ADHD symptomatology than to general psychopathological burden.

I ntroduction: Prospective memory (PM) deficits in children with attention-deficit/hyperactivity disorder (ADHD) significantly impact academic and daily functioning. Through two experiments, this study investigated how cognitive load and encoding strategies modulate PM performance. Methods: Experiment 1 included 43 children (21 ADHD, 22 typically developing) who completed an n-back task under high and low cognitive load. Experiment 2 included 44 children with ADHD who were randomly assigned to either a standard encoding group or an implementation intention encoding group, also completing the n-back task under both load conditions. Results: Experiment 1 showed that children with ADHD had significantly lower PM accuracy than typically developing peers. Signal detection analysis revealed that this deficit stemmed from a more conservative response bias rather than impaired perceptual sensitivity. Unexpectedly, PM accuracy and perceptual sensitivity were higher under high cognitive load than low load for both groups. Experiment 2 demonstrated that implementation intention encoding significantly enhanced PM accuracy and perceptual sensitivity in children with ADHD, with stable effects across load conditions and no interference with ongoing task performance. Discussion: These findings indicate that PM deficits in children with ADHD reflect a conservative response strategy rather than an inability to detect target cues. Implementation intention encoding provides an effective, load-independent cognitive strategy for enhancing PM performance. These results offer novel insights into the cognitive mechanisms underlying PM deficits in ADHD and provide evidence-based guidance for targeted interventions.

Early-life stress elevates the risk of developing neuropsychiatric disorders. However, the mechanism underlying this vulnerability, and how they contribute to sex differences in these disorders, remain to be understood. Here, we use multivariate brain-based predictive models to examine how the number, positive or negative appraisal, and impact of adolescent stressful life events reported either by the youth or their caregivers are reflected in neuroanatomy (cortical thickness, surface area, cortical and subcortical gray matter volume, and T1 intensity measures). We used data from the Adolescent Brain Cognitive Development (ABCD) study at 2-year (N = 6,301, age 11-12), 4-year (N = 5,000, age 13-14) and 6-year (N = 3,226, age 15-16) follow-up time points to examine the sex-independent and sex-specific neural correlates of stressful life events. Our analyses showed mostly non-significant associations between stressful life events and neuroanatomy. However, we did find that the number of positively appraised stressful life events reported by the caregivers at the 4-year follow-up was significantly associated with cortical thickness, independent of sex, and with surface area in females only. Across three developmental timepoints, seven neuroanatomical measures, two reporting perspectives, and both sex-independent and sex-specific analyses, we show that the number, appraisal, and impact of stressful life events are largely not reflected in adolescent neuroanatomy.

ImportancePrenatal exposure to gestational diabetes mellitus (GDM) has been associated with adverse metabolic, neurodevelopmental, and psychiatric outcomes in offspring. However, whether GDM-exposed youth exhibit heterogeneous neuroanatomical patterns remains unclear. ObjectiveTo identify distinct cortical thickness subtypes among GDM-exposed youth and examine their associations with anthropometric, neurocognitive, psychiatric/behavioral and neuroimaging measures both cross-sectionally and longitudinally. Design, Setting, and ParticipantsThis cohort study used the Adolescent Brain Cognitive Development (ABCD)(R)data, a multisite longitudinal population study. Subtype and Stage Inference (SuStaIn), an unsupervised machine learning framework, was applied to cross-sectional structural MRI data to identify cortical thickness patterns in 573 GDM-exposed youth and 2854 healthy controls. Posthoc longitudinal analyses included 1,853 observations from a subset of GDM-exposed youth with 1-, 2-, and 4-year follow-up visits to examine subtype differences in developmental trajectories over time. Exposure(s)Prenatal exposure to GDM. Main Outcome(s) and Measure(s)The primary outcomes included identification of cortical thickness subtypes and their inferred regional ordering patterns. Secondary outcomes included subtype-specific anthropometric, neurocognitive, psychiatric/behavioral and neuroimaging measures. ResultsThe GDM-exposed sample had a mean age of 119.02 {+/-} 7.34 months and was 47.5% female. Two cortical thickness subtypes were identified. Between subtypes, Subtype 1 (63.2%) was characterized by earlier inferred insula involvement and was associated with greater height (d = 0.36, pFDR < 0.001) and weight (d = 0.26, pFDR = 0.007), whereas Subtype 2 exhibited earlier inferred frontal involvement and nominally higher Attention-Deficit/Hyperactivity Disorder (ADHD) prevalence (d = 0.08, p = 0.036), steeper longitudinal cortical thinning across all six cortical regions of interest ({beta} range: -0.05 to -0.13, all pFDR < 0.05), and a smaller decline in Obsessive-Compulsive Disorder (OCD) prevalence over time ({beta} = -1.02, pFDR = 0.049). Conclusions and RelevanceGDM exposure was associated with two distinct offspring cortical thickness subtypes, each showing different inferred regional ordering patterns and clinical associations. One subtype showed an insula-cingulate-predominant pattern associated with anthropometric measures, whereas the other showed a frontal-predominant pattern associated with nominally higher psychiatric measures and faster cortical thinning over time.

BackgroundEarly adolescence is a common period of onset for depressive symptoms. In part, this may reflect a developmental manifestation of individuals genetic propensities as they undergo physiological and hormonal changes and interact with new environments. Many commonly proposed mechanisms assume direct effects of an individuals own genes on emerging variation in their depressive symptomatology. However, estimates of genetic influence based on analyses in unrelated individuals capture not only direct genetic effects but also genetic effects from parents and other biologically related family members. AimIn data from the Norwegian Mother, Father and Child Cohort (MoBa), we used linear mixed models to distinguish developmentally-stable and adolescence-specific direct and parental indirect genetic effects. We examined effects of polygenic scores for major depressive disorder (MDD), ADHD, anxiety disorders, and educational attainment (EA) on depressive symptoms, which were assessed by maternal reports at ages 8 and 14. ResultsChildrens own MDD polygenic scores showed adolescence-specific effects on depressive symptoms ({beta}PGS*wave=0.041, [95% CI: 0.017, 0.065]). Developmentally-stable direct effects from childrens polygenic scores for MDD ({beta}=0.016, [0.006, 0.039]), ADHD ({beta}=0.024, [0.008, 0.041]) and EA ({beta}=-0.02, [-0.038, -0.002]) were also evident. The only evidence of indirect genetic effects was a stable effect of maternal EA polygenic scores ({beta}=0.04, [0.024, 0.054]). ConclusionDirect genetic effects linked to genetic liability to MDD accounted for emerging variation in depressive symptoms in adolescence. These results imply that specific etiological mechanisms related to MDD may become particularly relevant for depressive symptoms during early adolescence compared to at earlier ages.

It has been proposed that bilinguals have better executive function (EF) arising from the constant selection of one language while inhibiting the other, and gray matter has been found to differ in bilinguals in regions linked to EF (frontal-parietal and subcortical structures). Attention Deficit Hyperactivity Disorder (ADHD) is associated with poorer EF and neuroanatomical differences underlying EF. Given the EF advantage in bilinguals, we investigated whether a bilingual experience affects EF performance and brain structure differentially in those with ADHD. Using the Adolescent Brain and Cognitive Development Study, we compared early Spanish-English bilinguals and English-speaking monolinguals with and without ADHD. ANOVAs for the Flanker, Working Memory, and Card Sort Tasks revealed no main effects of Language Experience (Bilingual versus Monolingual), a main effect of Diagnostic Group for Card Sort (ADHD worse than Controls), and no interaction effects on performance for any task. ANOVAs for gray matter volume (GMV) revealed a main effect of Language Experience in many regions, a main effect of Diagnostic Group in some regions, but no interactions. GMV in left thalamus was affected by both ADHD and bilingualism, but the effect of ADHD was not significantly diminished or enhanced by the dual-language experience. For cortical thickness, there was a main effect of Language Experience in several regions, no main effect of Diagnostic Group, and no interactions. Taken together, bilingualism has some impact on EF performance, a strong impact on neuroanatomy, but there was no disproportionate impact by bilingualism on the differences caused by ADHD for any measure. Research HighlightsExecutive function and brain structure differ in ADHD and in bilinguals, prompting the need to investigate interactive effects. Bilingualism did not disproportionately affect performance differences in ADHD for executive function, nor for gray matter volume or for cortical thickness differences in ADHD. Gray matter volume was less in ADHD than non-ADHD, as well as greater in bilinguals than monolinguals in the left thalamus, but without interaction effect. These independent effects indicate that the brain basis of ADHD is not impacted by a dual-language experience.

Children exposed to severe childhood maltreatment often develop complex mental health disorders where standard treatments show limited efficacy. Current residential approaches combine psychopharmacological with behavioural interventions, yet the feasibility and clinical-neurobiological outcomes of intensive, medication-free psychotherapy have not been investigated in this population. Our prospective study followed severely traumatized children (aged 6-13 years) with documented histories of changes and failures in placement.They completed an intensive 6-8 months inpatient treatment program (5 individual psychotherapy and 3 group therapy sessions per week with high caregiver-patient ratio) grounded in a novel, multimodal, attachment-based therapeutic framework. Medication was discontinued prior to treatment. The intervention group was compared to healthy controls and waitlist controls receiving treatment as usual. Participants in the intervention group achieved high remission rates for dysregulated behaviour (Child Behaviour Checklist (CBCL) >60% post treatment, 50% on follow-up) and trauma-related symptoms (Parent Report of Post-traumatic Stress Symptoms (PROPS) >65% post treatment, >60% on follow-up). Within-group effect sizes for Total Problems Score, Externalising behaviour (both CBCL), Hyperactivity (Strengths and Difficulties Questionnaire) and trauma symptoms (PROPS) each exceeded Cohen's d = 1.0 and were maintained at 6-month follow-up. Resting-state fMRI identified significant functional reorganization in visual processing networks. Atypical correlation patterns between visual network activity and symptom severity resolved following treatment, yielding patterns comparable to those of healthy controls. These pilot findings provide initial evidence of the feasibility and effectiveness of intensive, medication-free, attachment-based inpatient treatment to promote clinical remission and neurobiological normalization in severely traumatized children.

Background: Major depressive disorder (MDD) is the leading cause of non-fatal disability in youth and disproportionately affects adolescent females. Structural MRI studies of adolescent depression have yielded inconsistent findings, potentially reflecting symptom heterogeneity and rapid developmental changes in brain morphology. Methods: In this longitudinal study, we examined associations between specific depressive symptoms and structural brain MRI measures in 9,722 youth (53% male, age range = 10.0-17.7, 24,378 observations) from the Adolescent Brain Cognitive Development (ABCD) Study. A four-wave panel graphical vector autoregression (GVAR) model was estimated to separate within-person (contemporaneous and temporal networks) from stable between-person effects. Brain measures included cortical thickness in the insula, cingulate, medial orbitofrontal cortex (mOFC) and fusiform gyrus, as well as hippocampal volume. Depressive symptoms included parent-reported depressed mood, anhedonia, lethargy, and worthlessness. Additionally, sex-differences in network structures were tested. Results: Strong within-domain associations were observed among brain measures and among symptoms, with the largest effects in the symptom domain. Cross-domain (brain-symptom) associations emerged only at the within-person level, where elevated depressed mood was associated with contemporaneous and subsequent reductions in cingulate and fusiform gyrus thickness (partial r = [-0.02 - 0.04]). No cross-domain associations were detected in the between-person networks. Sex-differences emerged only in the within-person networks. Conclusions: Associations between brain structure and depressive symptoms were subtle, symptom-specific, and dynamic rather than reflecting stable individual differences. Longitudinal within-person approaches are therefore important for understanding neurodevelopmental contributions to adolescent depression risk.

Abstract Parental depression and early child neurodevelopment are closely interconnected, yet few population-based studies have examined both maternal and paternal depression in relation to early neurodevelopmental risk. This study aimed to examine the association between child neurodevelopmental risk and parental depression in the French national birth cohort Etude Longitudinale Francaise depuis l'Enfance (ELFE). We conducted a cross-sectional analysis of 12,953 children and their parents who participated in the 2-year follow-up. Child neurodevelopmental risk was assessed at age 2 years using the Modified Checklist for Autism in Toddlers and categorized as low, intermediate, or high risk. Parental depression was assessed using the Kessler Psychological Distress Scale and defined as maternal depression, paternal depression, or depression in at least one parent. Multivariable logistic regression models were adjusted for sociodemographic, pregnancy-related, and child characteristics. Compared with low child neurodevelopmental risk, intermediate risk was associated with higher odds of maternal depression and depression in at least one parent. High child neurodevelopmental risk was associated with substantially higher odds of maternal depression and depression in at least one parent. Associations with paternal depression were weaker and were no longer statistically significant after adjustment. These findings suggest that parental depression, particularly maternal depression, is associated with early child neurodevelopmental risk from the stage of initial developmental concerns. They support an integrated, family-centred approach combining early identification of child developmental vulnerability with attention to parental mental health.

Adolescence is a critical period for the development of the brain, cognition, and mental health, which are shaped by a wide range of environmental factors. In the present study, we analysed the Adolescent Brain and Cognitive Development (ABCD) dataset to examine how a range of proximal (e.g., socioeconomic status, familial circumstances) and distal (e.g., neighbourhood conditions, access to healthcare and education) environmental factors are associated with changes in centile-based measures of brain structure, and whether these brain differences subsequently mediate variations in cognition and mental health. We analysed these associations both at baseline (N = 6,911; 3,605 M, 3,606 F; mean age = 9.93) and longitudinally across three timepoints (N = 1,628; 879 M, 749 F; ages 8-15). At baseline, a more advantaged proximal and distal environment was associated with larger volumes across the whole brain relative to age- and sex-matched peers, which, in turn, mediated better mental health outcomes and cognitive performance. In the longitudinal analysis, the childhood environment predicted changes in brain structure across adolescence, and these structural changes predicted changes in mental health and cognition. The childhood environment also predicted cognitive but not mental health changes across adolescence, suggesting that these associations may already be established early in adolescence. These findings provide insight into how environmental and neural factors shape adolescent mental health and cognition, with potential implications for early intervention strategies aimed at promoting positive developmental outcomes.

BackgroundEmotional and cognitive difficulties often co-occur in neurodevelopmental conditions. While transdiagnostic, dimensional approaches offer a more precise framework for understanding mental health than diagnostic categories, their neural correlates in youth with learning difficulties remain poorly understood. This study investigates associations between transdiagnostic mental health dimensions and resting-state functional connectivity in struggling learners. MethodsCross-sectional behavioural data from the Centre for Attention, Learning and Memory (CALM) for struggling learners (N = 378) was used to replicate a hierarchical model of mental health from the Conners Parent Rating Short Form, the Revised Childrens Anxiety and Depression Scale and the Strengths and Difficulties Questionnaire. Functional connectomes were derived from resting-state fMRI data (N = 67), and partial least squares regression related mental health dimensions to connectivity within and between large-scale brain networks. ResultsThe replicated model comprised a general p-factor, two broad domains (internalising and externalising), and three specific dimensions (specific internalising, neurodevelopmental and social maladjustment). Symptom severity was associated with two connectivity patterns: greater default mode network coupling to frontoparietal and attention networks, and reduced connectivity between visual and somatomotor systems. These effects were strongest for the neurodevelopmental and social maladjustment dimensions, respectively. ConclusionsThese findings align with population-level evidence linking mental health dimensions to brain network organization, extending it to struggling learners and offering new insight into the neural basis of mental health vulnerability in neurodevelopmentally at-risk youth.

Importance: Parent/caregiver-infant early relational health (ERH) is known to play a critical role in the promotion of socio-emotional functioning and wellbeing across the life course. The negative impact of the COVID-19 pandemic on maternal mental health and secondarily on ERH and child socio-emotional functioning is clear. However, the direct impact of maternal viral exposure during pregnancy on ERH has not been investigated. Objective: The goal of this study was to determine the impact of prenatal SARS-CoV-2 exposure on ERH and infant socio-emotional functioning in the first 6 months of life. Design: Mothers with and without SARS-CoV-2 exposure during pregnancy who gave birth from 02/2020 to 09/2021 were enrolled from 05/2020 to 09/2021 in one of two parallel prospective studies (the COVID-19 Mother Baby Outcomes [COMBO] Initiative or the Respiratory Syndrome Coronavirus 2 in Pregnancy and Infancy [ESPI] COMBO sub-study). Mothers reported on their health and the socio-emotional functioning of their infant via online surveys (REDCap) at enrollment, 1, 2, 4, and 6 months. At 4 to 6 months, dyads were invited to participate in a video-based, remote assessment of ERH. Participants: 884 mother-infant dyads from three U.S. States (Alabama, New York, and Utah). Exposure: Prenatal SARS-CoV-2. Main Outcomes and Measures: Maternal-reported ERH (parental stress, parenting confidence and bonding) and observer-based ERH (video-coded quality of maternal caregiving behaviors and mother-infant emotional connection). Infant socio-emotional development assessed using the 6-month Ages and Stages Questionnaire: Socio-Emotional 2nd Edition (ASQ:SE-2). Results: 316 (36%) mothers had a positive prenatal SARS-CoV-2 exposure. Prenatal SARS-CoV-2 exposure was associated with an adjusted estimate of ~5% reduction (incidence rate ratio=0.95, 95% confidence interval [0.90, 1.00], p=0.03) in observed maternal caregiving quality, after accounting for postnatal maternal mental health and sociodemographic factors. We found no evidence of effect on other ERH constructs or infant socio-emotional functioning. Conclusions and Relevance: In this large prospective cohort study, prenatal SARS-CoV-2 was associated with a small decrement in caregiving quality, but not other ERH constructs or infant socio-emotional functioning. These findings should be interpreted as hypothesis generating and will require replication in independent studies.