Background

People with early-life experiences of deprivation are more likely to develop psychotic symptoms. While the mechanisms of this relationship are poorly understood, research suggests a role of cortical development.

Methods

In 6323 youth from the Adolescent Brain Cognitive Development study, we examined associations between total, material, interpersonal, cognitive and neighbourhood deprivation at age 9–11 years and psychotic-like experiences (PLEs) 2 years later. We then investigated whether associations were mediated by variation in cortical volume at baseline or rate of change from baseline to follow-up. Sex-specific effects were examined throughout.

Results

All deprivation measures were associated with greater PLEs. Most of these associations were partially mediated by variation in cortical structure in widespread regions, including lower baseline cortical volume in ventral visual and sensorimotor regions and particularly in females, steeper cortical volume decline in association areas.

Conclusions

Early-life deprivation may be associated with psychotic-like experiences via disruption to cortical structure. This phenomenon is common to several forms of deprivation and continues into early adolescence in certain regions.

Background

Whether, and how, infant characteristics and parenting quality interact is one of developmental psychology's key questions. However, whether specific interaction patterns replicate across cohorts or developmental outcomes is largely unknown. This study investigates whether infant characteristics and parenting quality are independent predictors (additive effects) of child outcomes or interact such that certain infants particularly suffer from poor parenting (diathesis stress), particularly benefit from good parenting (vantage sensitivity) or both (differential susceptibility).

Methods

Individual participant data from over 30,000 children from four prospective cohorts were pooled. Using a competitive-confirmatory approach of model evaluation, 16 possible permutations of infant characteristics (temperament and birthweight), parenting (maternal-reported stimulating and sensitive parenting) and later developmental outcomes (fluid and crystalised intelligence, internalising and externalising behaviour) were tested. The robustness of results was evaluated by subsequently varying analytic methods, using alternative parenting measures including observer reports and excluding covariates.

Results

AIC values in 10/16 analyses indicated infant characteristics acted independently of maternal-reported parenting for predicting developmental outcomes. Interaction patterns indicating diathesis stress (4/16), vantage sensitivity (2/16) or differential susceptibility (0/16) were rare or absent. However, diathesis-stress patterns were frequently found regarding birthweight and internalising behaviours, which were largely robust to methodological changes.

Conclusions

Developmental outcomes are more consistently explained by additive effects rather than by interaction effects.

Background

Error monitoring, a neurocognitive process reflecting self-detection of errors, has been proposed as a marker of social anxiety. However, the way in which this marker relates to social anxiety is not consistent across age, as older children and adolescents with anxiety exhibit heightened error monitoring and younger children with anxiety exhibit diminished error monitoring. One way to contextualize this inconsistency and provide insight into childhood social anxiety is to examine the less-studied consequences of error monitoring, termed post-error processing.

Methods

We employed computational modeling to estimate a form of post-error processing (attentional focusing) during a flanker task, within a cross-sectional sample of 148 treatment-seeking youth aged 7–17. Youth reported social anxiety symptoms via the Screen for Child Anxiety Related Disorders (SCARED).

Results

Mixed-effects regression analyses revealed a three-way interaction (p = .034) between trial type (post-error/correct), age, and social anxiety symptoms predicting attentional focusing. Higher social anxiety predicted diminished post-error attentional focusing in children, but this effect changed across age, with higher social anxiety no longer predicting diminished post-error attentional focusing by adolescence.

Conclusions

Studying the functional consequences of committing errors (post-error processing) provides additional context for understanding the relationship between social anxiety and error monitoring. These data elucidate important changes in the relationship between social anxiety and post-error processing across age and could therefore inform developmentally sensitive treatments of pediatric social anxiety.

Background

Empirical evidence supports the efficacy of behavioral online parent training. However, further large trials in school-age children with externalizing behavior problems and analyses on the impact of additional therapist support are needed. This three-arm randomized controlled trial examined the efficacy of guided and unguided web-assisted self-help (WASH) for parents of children with externalizing behavior problems.

Methods

Parents of 431 children (6–12 years) with elevated externalizing symptoms were randomly assigned to either treatment as usual (TAU), a 6-month behavioral WASH intervention (WASH+TAU), or WASH plus telephone-based support (WASH+S+TAU). Assessments took place at baseline and at 3, 6, and 12 months. The primary outcome was child externalizing symptoms as rated by a clinician blinded to condition; secondary outcomes were parent-rated child externalizing symptoms, internalizing symptoms, functional impairment, quality of life, parenting practices, and parental internalizing symptoms. (German Clinical Trials Register (DRKS): DRKS00013456; URL: https://drks.de/search/de/trial/DRKS00013456; registered on January 3rd 2018).

Results

Linear mixed models for repeated measures revealed a significant overall intervention effect on blinded clinician-rated externalizing symptoms at 6 months in both the intention-to-treat sample and per-protocol samples, with at least 25% (PP25) or 40% treatment utilization (PP40), respectively (intention-to-treat: p = .017). Subsequent pairwise comparisons revealed a greater symptom reduction in WASH+S+TAU than in the other conditions (intention-to-treat: WASH+S+TAU vs. WASH+TAU: p = .029, d = −0.28, 95% CI [−0.54, −0.03]; WASH+S+TAU vs. TAU: p = .009, d = 0.34 [−0.59, −0.09]). At 12 months, a significant overall effect on blinded clinician-rated externalizing symptoms only emerged in the PP40 sample (p = .035). Secondary analyses revealed an overall effect on child functional impairment at 12 months (intention-to-treat and per-protocol analyses) and on negative parenting behaviors at 6 months in the PP40 sample. For both variables, pairwise comparisons demonstrated significant differences between WASH+S+TAU and TAU.

Conclusions

Parent-directed WASH is effective in reducing blinded clinician-rated externalizing symptoms, but only when combined with additional support.

Background

The present study sought to extend the existing knowledge on the relationship between risky behavior and ADHD by studying transactions between these two variables within participants and across various time scales.

Methods

Participants were 281 adolescents (170 girls), age 13–18 years old (M = 14.8, SD = 1.3), and 1 of their parents. Risky behavior and ADHD symptoms measurements were taken at varying time intervals: annually, 4-monthly, and weekly. Random Intercepts Cross-Lagged panel modeling (RI-CLPM) was used to examine longitudinal bidirectional associations between risky behavior and ADHD symptoms.

Results

At the between-person level, positive associations between risky behavior and ADHD symptoms were found in all time scales. At the within-person level, according to adolescents' reports, ADHD symptoms did not predict subsequent fluctuations in adolescents' risky behavior, though according to parental reports on adolescents' risky behaviors, a cross-lagged effect of risky behaviors on ADHD symptoms was evident in the annual time scale.

Conclusions

Between-person relations between ADHD and risky behavior were established, suggesting an underlying common factor. Within-person relations were suggested only in parent reports and specific time scales. Our research underscores the critical need to differentiate between inter-individual and intra-individual effects when investigating the interplay between ADHD and risky behavior over time.

Background

Infants vary significantly in the way they process and respond to sensory stimuli, and altered sensory processing has been reported among infants later diagnosed with autism. Previous work with adolescents and adults suggests that variability in sensory processing may have a strong genetic basis. Yet, little is known about the etiological factors influencing sensory differences in infancy, when brain circuits supporting social and non-social cognition are sculpted and learning about the world via sensory input largely occurs in interaction with caregivers.

Methods

We analysed data from a community sample of monozygotic (MZ) and dizygotic (DZ) 5-month-old same-sex twins (n = 285 pairs, n = 158 MZ pairs, n = 150 male pairs) from the BabyTwins Study in Sweden (BATSS) using exploratory factor analysis, generalised estimating equations and multivariate twin models to delineate the phenotypic and etiological structure of individual variability across different sensory processing dimensions, as measured by the Infant/Toddler Sensory Profile. Developmental links to later autistic traits were also assessed, as measured by total scores from the Quantitative Checklist for Autism in Toddlers at 36 months.

Results

Results suggested separability between sensory processing dimensions (i.e. sensation seeking, sensation avoiding, sensory sensitivity and low registration) at a phenotypic and etiological level, with significant contributions from additive genetics and family environment that were unique to each sensory dimension and significant but smaller contributions from shared influences. Sensory domains also showed etiological separability, with unique genetic influences to each domain, while contributions from shared environment were in part shared across domains. A higher incidence of tactile-related behaviours and behaviours associated with sensory sensitivity, sensation avoiding, and low registration were significantly associated with higher levels of autistic traits in toddlerhood.

Conclusions

This study provides a map of the phenotypic and etiological structure of sensory processing in infancy, which will be informative for studies of both typical and atypical development.

Background

Exposure to trauma in childhood is associated with an increased risk for internalising symptoms. Alterations in pubertal development has been proposed as a potential mechanism underpinning this association. However, longitudinal studies, which are needed to examine pubertal development over time, are scarce. The goal of this pre-registered study was to examine how trauma exposure shapes the timing and tempo of pubertal development, and in turn contributes to risk for internalising symptoms in female youth.

Methods

Using the largest longitudinal sample to date, we characterised profiles of pubertal development across four time points in female youth from the Adolescent Brain Cognitive Development (ABCD) Study (N = 4,225, age range = 9–14 years) using latent profile analysis. Pubertal development was assessed using the Pubertal Development Scale (at four time points). Trauma exposure was quantified using the post-traumatic stress disorder subscale from the parent-report Kiddie Schedule for Affective Disorders and Schizophrenia for DSM-5 (at baseline), and internalising symptoms were assessed using the self-report Brief Problem Monitor (at 3-year follow-up).

Results

Pubertal development could be grouped into three latent classes: early starters (9% of sample), typical developers (76%) and slow developers (15%). The early starters demonstrated higher levels of trauma exposure compared to typical developers and slow developers, while slow developers showed the least exposure to trauma. Youth with greater exposure to trauma were at an increased risk for internalising symptoms at ages 12–14 years, and this association was mediated by a higher pubertal status at ages 9–10 years, but not by a faster pubertal tempo.

Conclusions

Accelerated pubertal development, characterised by an earlier age of onset but not a higher pubertal tempo in the transition from late childhood to early adolescence, may be a mechanism through which trauma exposure in childhood increases risk for internalising symptoms in female youth.

Blader et al.'s (2025) recent annual review article makes an important contribution to the literature on emotion dysregulation in child and adolescent mental health. In addition to synthesizing the current evidence base, the authors put forth a cogent formalized view of emotion regulatory processes and how they go awry. Much has been written on emotion (dys)regulation and psychopathology (for overviews, see Lincoln et al., 2022; Paulus et al., 2021; Sheppes et al., 2015). It would therefore be reasonable to ask what novel contribution could be made by a new review article at this time. But for all that has been written, there is much work still to be done. Blader et al. (2025) admirably rise to meet this challenge. We hope this commentary amplifies and adds to their effort. Below, we reflect on a few aspects of their contribution and offer some further thoughts that may inform future work in this area.

Background

Autistic individuals often receive psychiatric diagnoses prior to their autism diagnosis. It remains unclear to what extent autistic females and males differ in their likelihood of receiving psychiatric diagnoses prior to their autism diagnosis and continue seeking care for them after an autism diagnosis.

Methods

In a nationwide cohort of all individuals born in Sweden 1990–2015 with a clinical autism diagnosis (N = 72,331, n _females = 24,110), we used linear and logistic regression to estimate the association between sex and (a) psychiatric diagnoses before autism diagnosis, including time trends by autism diagnosis year (2010–2020), (b) autism diagnosis age in those with preceding diagnoses, (c) stability of preceding diagnoses (defined as continued care utilization indicated through diagnosis or medication in the 5 years following autism diagnosis).

Results

In total 54.2% of autistic females and 40.9% of autistic males received at least one preceding psychiatric diagnosis (most common: ADHD, anxiety, depression). Autistic females showed higher odds than males for most preceding psychiatric diagnoses (OR_range = 1.29 [1.18, 1.41]–10.69 [8.06, 14.17]), except psychotic disorders (OR = 0.91 [0.78, 1.06]) and ADHD (OR = 0.69 [0.66, 0.71]). Sex differences in preceding diagnoses were persistent across different autism diagnosis years (2010–2020). For most conditions, females with a preceding diagnosis were diagnosed with autism later than males with the same condition. For both sexes, the stability of preceding diagnoses varied considerably (23.1%–88.9%) and was less than 50% for most diagnoses. Females showed a higher stability for anxiety, sleep disorders and self-harm (OR_range = 1.45 [1.30, 1.62]–2.37 [1.93, 2.90]), and males for psychotic disorders (OR = 0.60 [0.44, 0.81]).

Conclusions

Autistic females are more likely to be diagnosed with psychiatric conditions prior to an autism diagnosis and receive care for them post autism diagnosis. Our findings emphasize the variability of clinical presentation and importance of disentangling persistent support needs from overlapping diagnostic presentations, particularly in autistic females, to provide appropriate and timely care.

The spectrum of psychosis is highly relevant to child and adolescent mental health. Psychotic symptoms are common in children and adolescents. The onset of psychotic disorders is often preceded by neurodevelopmental problems in early childhood, and some 13% of adolescents attending specialist mental health services will later be diagnosed with a psychotic disorder or bipolar disorder. Although 12% of psychotic disorders and 8% of schizophrenia cases have onset prior to age 18, there is little evidence available to guide the clinical care of young people with early onset psychosis. This commentary summarises the key findings of the annual research review on Psychosis in Children and Adolescents. It highlights the urgent need for clinicians and researchers in child and adolescent mental health to contribute to finding solutions to prevent the onset of psychosis and improve the lives of young people with early onset psychosis and their families.

Background

Certain temperament characteristics, such as low effortful control and high negative affectivity, are linked to an elevated likelihood for later psychopathology. Although genetic vulnerability has been associated with a number of psychiatric conditions, little work has examined the genetic architecture underlying temperament or the genetic overlap between early temperament profiles and later mental health outcomes. The present study examined associations of polygenic scores for anxiety (PGS-Anxiety) and ADHD (PGS-ADHD) with temperament characteristics in a longitudinal sample of children assessed from infancy through age 7 years.

Methods

Analyses were conducted in a sample of children (European Ancestry n = 476; Full Sample [European and other ancestries] N = 606).

Results

We observed an age-by-PGS interaction on effortful control. As children aged, there appeared to be stronger negative associations between PGS-ADHD and effortful control. No associations were observed between PGS-Anxiety and negative affectivity.

Conclusions

Overall, the findings suggest some support for associations between genetic underpinnings for externalizing psychopathology and temperament that increase over time.

Background

Dyslexia is one of the most common neurodevelopmental disorders. There have been many definitions over the past century, and debate continues as to how dyslexia should be defined. This debate contributes to confusion and misinformation. We move beyond the debate by establishing areas of consensus among a wide range of experts.

Methods

We conducted a Delphi study with a panel of dyslexia experts, including academics, specialist teachers, educational psychologists, and individuals with dyslexia, asking them for their views on a set of key statements about dyslexia. We carried out two survey rounds, in each case accepting statements with greater than 80% consensus and reviewing and revising other statements using feedback from the expert panel. This was followed by discussion with a subset of the panel around a few statements with marginal consensus.

Results

Forty-two statements were ultimately accepted. In the current paper we review those statements that pertain to a definition of dyslexia, demonstrate how they align with the research literature, and build on previous definitions of dyslexia.

Conclusions

There was considerable consensus in our expert panel that dyslexia is a difficulty in reading and spelling, associated with multiple factors, and that it frequently co-occurs with other developmental disorders. It was agreed that difficulties in reading fluency and spelling are key markers of dyslexia across different ages and languages. We conclude with a proposed new definition of dyslexia.

It was early 2020, a week or two into Hilary Term, what everyone else calls Spring Term, but we at Oxford love our arcane traditions. I recall one of my graduate students, from China, coming to me ashen-faced at the end one of my lectures on the effects of bilingualism on the linguistic and cognitive development of young learners. “Please be careful,” she said. “Have you heard about the disease. It's really scary. Please look after your family.” Over the preceding Christmas break, news had started to filter through about a new form of flu that had spread rapidly from Wuhan in Eastern China to other parts of the country and was now starting to emerge in other parts of the world. We were starting to see desperate images of enforced quarantine, coerced separation of infected individuals from their loved ones, the rapid construction of temporary hospitals to house the unwell, and of course, school closures. It didn't look good. But I had seen similar outbreaks in the past. I had been working in Southeast Asia during the avian flu epidemic of 2003–04, and I was still there when swine flu broke out in 2009. Both were worrying, but neither had come to anything that could be classified as universally threatening. The school where I worked sent colleagues and children to be tested at the first sign of a tickly throat or stuffy nose, and a strict and regular cleaning and hand sanitising regime was implemented.

Jaffee and colleagues present a masterful review of the evidence for the impacts of cash transfer programmes on child and adolescent mental health in the United States. While global meta-analyses find evidence of effectiveness, Jaffee and colleagues highlight the limited number of studies in Northern America, but find overall results indicating small but meaningful effect sizes on improving emotional and behavioural health, and greatest impacts for the poorest families.

Research on Adverse Childhood Experiences (ACEs) has progresses at a rapid pace over the last 30 years and publications now span many fields and disciplines. With a literature this vast, it is important to stake stock of what is known and where gaps in knowledge remain by reviewing and synthesizing published findings. In this commentary, I center remarks on a well-designed umbrella review conducted by Kim et al. on the impact of ACEs. Their review adds depth and precision to earlier reviews on this topic and draws attention to areas where further research is needed, including mechanisms underlying the transmission of risk and the onset of health-related outcomes associated with ACE exposure. I conclude the commentary by echoing a call by Kim and colleagues for more investment in public health prevention to reduce ACE exposure, lessen trauma symptoms, and reduce costs to society.

Proliferation of the term “emotion dysregulation” in child psychopathology parallels the growing interest in processes that influence negative emotional reactivity. While it commonly refers to a clinical phenotype where intense anger leads to behavioral dyscontrol, the term implies etiology because anything that is dysregulated requires an impaired regulatory mechanism. Many cognitive, affective, behavioral, neural, and social processes have been studied to improve understanding of emotion dysregulation. Nevertheless, the defective regulatory mechanism that might underlie it remains unclear. This systematic review of research on processes that affect emotion dysregulation endeavors to develop an integrative framework for the wide variety of factors investigated. It seeks to ascertain which, if any, constitutes an impaired regulatory mechanism. Based on this review, we propose a framework organizing emotion-relevant processes into categories pertaining to stimulus processing, response selection and control, emotion generation, closed- or open-loop feedback-based regulation, and experiential influences. Our review finds scant evidence for closed-loop (automatic) mechanisms to downregulate anger arousal rapidly. Open-loop (deliberate) regulatory strategies seem effective for low-to-moderate arousal. More extensive evidence supports roles for aspects of stimulus processing (sensory sensitivity, salience, appraisal, threat processing, and reward expectancy). Response control functions, such as inhibitory control, show robust associations with emotion dysregulation. Processes relating to emotion generation highlight aberrant features in autonomic, endocrine, reward functioning, and tonic mood states. A large literature on adverse childhood experiences and family interactions shows the unique and joint effects of interpersonal with child-level risks. We conclude that the defective closed-loop regulatory mechanisms that emotion dysregulation implies require further specification. Integrating research on emotion-relevant mechanisms along an axis from input factors through emotion generation to corrective feedback may promote research on (a) heterogeneity in pathogenesis, (b) interrelationships between these factors, and (c) the derivation of better-targeted treatments that address specific pathogenic processes of affected youth.

Background

Early identification of bipolar disorder (BD) provides an important opportunity for timely intervention. In this study, we aimed to develop machine learning models using large-scale electronic health record (EHR) data including clinical notes for predicting early-onset BD.

Methods

Structured and unstructured data were extracted from the longitudinal EHR of the Mass General Brigham health system. We defined three cohorts aged 10–25 years: (1) the full youth cohort (N = 300,398); (2) a subcohort defined by having a mental health visit (N = 105,461); and (3) a subcohort defined by having a diagnosis of mood disorder or ADHD (N = 35,213). By adopting a prospective landmark modeling approach that aligns with clinical practice, we developed and validated a range of machine learning models, across different cohorts and prediction windows.

Results

We found the two tree-based models, random forests (RF) and light gradient-boosting machine (LGBM), achieving good discriminative performance across different clinical settings (area under the receiver operating characteristic curve 0.76–0.88 for RF and 0.74–0.89 for LGBM). In addition, we showed comparable performance can be achieved with a greatly reduced set of features, demonstrating computational efficiency can be attained without significant compromise of model accuracy.

Conclusions

Good discriminative performance for models predicting early-onset BD can be achieved utilizing large-scale EHR data. Our study offers a scalable and accurate method for identifying youth at risk for BD that could help inform clinical decision-making and facilitate early intervention. Future work includes evaluating the portability of our approach to other healthcare systems and exploring considerations regarding possible implementation.

Maheux et al.s' annual review (2024) summarizes a rapidly evolving literature on the specific components (including content, features and functions) of social media that can help or hinder healthy adolescent development, highlighting how proposed effects of social media components appear to matter more for some adolescents than others. This commentary explores how conclusions of Maheux et al. (2024) can help shape future translational research on what components of social media may facilitate or undermine healthy adolescent development and who is most susceptible to these social media component effects. Future research must also address when and where social media components matter most, situating our understanding within temporal and physical context. Finally, the promise of future research is highlighted on why youth engage with social media components (motivations) and how specific components of social media exert their effects (mechanisms).

Background

The impact of maternal sleep disturbances during pregnancy on long-term neurodevelopment and the role of metabolites in this process are not well understood. In a prospective cohort study, we aimed to investigate the associations between maternal sleep disturbances during each trimester and child intelligence quotient (IQ) at the age of 4 years and to identify metabolites that might mediate these relationships.

Methods

This study included 1,870 mother–child pairs from the Shanghai Birth Cohort (SBC). Maternal sleep quality was assessed using the Pittsburgh sleep quality index (PSQI) questionnaire in the first and second trimesters, and a simplified version of the PSQI was used in the third trimester. Child IQ was evaluated at age 4 using the Wechsler Primary and Preschool Scale of Intelligence-Fourth Edition (WPPSI-IV). We conducted untargeted analyses of maternal serum metabolomics in the first trimester in 1,461 subjects. We employed multiple linear regression models to examine the associations between maternal sleep disturbances during each trimester and child IQ. Additionally, we utilized longitudinal latent class analysis (LLCA) to identify patterns of sleep quality changes throughout the three trimesters and employed multiple linear regression models to investigate how these sleep patterns across the entire pregnancy were associated with child IQ. We applied a ‘meet-in-the-middle’ approach to identify potential metabolites linking maternal sleep disturbances during early pregnancy with child IQ.

Results

Longer sleep latency was associated with lower child Full-Scale IQ (FSIQ) and verbal comprehension index (VCI) for the first trimester, while lower child fluid reasoning index (FRI) for the second trimester. Longer sleep latency throughout the pregnancy was associated with decreased FSIQ (β = −4.68; 95% CI: −8.32, −1.03), VCI (β = −6.38; 95% CI: −10.39, −2.37), and FRI (β = −4.29; 95% CI: −7.96, −0.63). We found that inositol, indoleacrylic acid, and 4-hydroxyquinoline emerged as potential biomarkers that play an intermediary role in the association between maternal sleep disturbances and child IQ.

Conclusions

Sleep disturbance during pregnancy may be a risk factor for compromised IQ in preschool-aged offspring. Alterations in inositol and tryptophan metabolism might be the mediator for the link between maternal sleep disturbances and child IQ.

Background

Anxiety and depression are highly prevalent in youth and can cause significant distress and functional impairment. The presence of maternal anxiety and depression are well-established risk factors for child internalizing psychopathology, yet the responsible mechanisms linking the two remain unclear.

Methods

We examined the potential mediating and moderating roles of EEG frontal alpha asymmetry (FAA) in the intergenerational transmission of internalizing symptoms in a longitudinal sample of N = 323 mother–child dyads. Self-report maternal internalizing symptoms were evaluated at child age 3 years and 5 years, child EEG at 5 years, and parent-report child internalizing symptoms at age 7 years. Mediation was evaluated via bootstrapped (N = 5,000) confidence intervals.

Results

We found significant associations among maternal internalizing (anxiety, depressive) symptoms when their children were ages 3 and 5 years, child FAA at age 5 years, and child internalizing symptoms at age 7 years. There was a significant mediation effect, whereby greater maternal anxiety and depressive symptoms at age 3 years were significantly associated with FAA (greater relative right cortical activation) in children at age 5 years, which, in turn, was significantly associated with greater child internalizing symptoms at age 7 years (ps < .001). There was no moderating effect of FAA on the association between maternal internalizing symptoms at age 5 years and child internalizing symptoms at age 7 years.

Conclusions

Greater right frontal asymmetry may be a neurophysiological mechanism that mediates the intergenerational transmission of internalizing symptoms.