Autism spectrum disorder (ASD) is a common neurodevelopmental disorder characterized by deficits in social communication and presence of restricted, repetitive behaviors, and interests. However, individuals with ASD vary significantly in their challenges and abilities in these and other developmental domains. Gene discovery in ASD has accelerated in the past decade, and genetic subtyping has yielded preliminary evidence of utility in parsing phenotypic heterogeneity through genomic subtypes. Recent advances in transcriptomics have provided additional dimensions with which to refine genetic subtyping efforts. In the current study, we investigate phenotypic differences among transcriptional subtypes defined by neurobiological spatiotemporal co-expression patterns. Of the four transcriptional subtypes examined, participants with mutations to genes typically expressed highly in all brain regions prenatally, and those with differential postnatal cerebellar expression relative to other brain regions, showed lower cognitive and adaptive skills, higher severity of social communication deficits, and later acquisition of speech and motor milestones, compared to those with mutations to genes highly expressed during the postnatal period across brain regions. These findings suggest higher-order characterization of genetic subtypes based on neurobiological expression patterns may be a promising approach to parsing phenotypic heterogeneity among those with ASD and related neurodevelopmental disorders.

To understand the complex relationships between autism spectrum disorder (ASD) and other frequently comorbid conditions, a growing number of studies have investigated the emergence of ASD during infancy. This research has suggested that symptoms of ASD and highly related comorbid conditions emerge from complex interactions between neurodevelopmental vulnerabilities and early environments, indicating that developing treatments to prevent ASD is highly challenging. However, it also suggests that attenuating the negative effects of ASD on future development once identified is possible. The present paper builds on this by conceptualizing developmental delays in nonsocial skills as the potential product of altered caregiver–infant interactions following the emergence of ASD during infancy. And, following emerging findings from caregiver–infant dyadic head-mounted eye-tracking (D-ET) research, it also suggests that a multiple pathway model of joint attention can provide mechanistic insights into how ASD alters the ability of caregiver and infant to create a context for infant learning. The potential for this view to inform early intervention is further discussed and illustrated through D-ET data collected prior to and following a brief, parent-mediated intervention for infant ASD. While promising, further research informing how a multiple pathway model of joint attention can inform ASD early intervention is needed.

Both preterm birth and early institutional deprivation are associated with neurodevelopmental impairment—with both shared and distinctive features. To explore shared underlying mechanisms, this study directly compared the effects of these putative risk factors on temperament profiles in six-year-olds: Children born very preterm (<32 weeks gestation) or at very low birthweight (<1500 g) from the Bavarian Longitudinal Study (n = 299); and children who experienced >6 months of deprivation in Romanian institutions from the English and Romanian Adoptees Study (n = 101). The former were compared with 311 healthy term born controls and the latter with 52 nondeprived adoptees. At 6 years, temperament was assessed via parent reports across 5 dimensions: effortful control, activity, shyness, emotionality, and sociability. Very preterm/very low birthweight and postinstitutionalized children showed similarly aberrant profiles in terms of lower effortful control, preterm = −0.50, 95% CI [−0.67, −0.33]; postinstitutionalized = −0.48, 95% CI [−0.82, −0.14], compared with their respective controls. Additionally, postinstitutionalized children showed higher activity, whereas very preterm/very low birthweight children showed lower shyness. Preterm birth and early institutionalization are similarly associated with poorer effortful control, which might contribute to long-term vulnerability. More research is needed to examine temperamental processes as common mediators of negative long-term outcomes following early adversity.

Bullying victimization is common in adolescence and has been associated with a broad variety of psychopathology and alcohol use. The present study assessed time-varying associations between bullying victimization and alcohol use through internalizing and externalizing symptoms and whether this indirect association throughout time is moderated by personality. This 5-year longitudinal study (3,800 grade 7 adolescents) used Bayesian multilevel moderated mediation models: independent variable was bullying victimization; moderators were four personality dimensions (anxiety sensitivity, hopelessness, impulsivity, and sensation seeking); internalizing symptoms (anxiety, depressive symptoms) and externalizing symptoms (conduct, hyperactivity problems) were the mediators; and alcohol use, the outcome. Results indicated significant between, within, and lagged effects on alcohol use through internalizing and externalizing symptoms. There were significant between and within effects on alcohol use through internalizing symptoms for adolescents with high anxiety sensitivity and hopelessness, and significant between, within, and lagged effects on alcohol use through externalizing symptoms for adolescents with high impulsivity and sensation seeking. These findings implicate two risk pathways that account for how bullying victimization enhances alcohol use risk and emphasize the importance of personality profiles that can shape the immediate and long-term consequences of victimization.

Greater maternal depressive symptoms are consistently associated with higher levels of behavioral difficulties in children, emerging in early childhood and with long-lasting consequences for children’s development. Interventions promoting early relational health have been shown to have benefits for children’s behavior; however, these impacts are not always realized in the context of maternal depression. This study examined whether tiered programs could address this limitation by focusing on both parenting, through universal primary prevention, and psychosocial stressors and parent mental health, through tailored secondary prevention. Analysis of a randomized controlled trial (RCT) of the Smart Beginnings (SB) intervention was conducted to determine whether SB attenuated the association between maternal depression and early childhood internalizing and externalizing behaviors. Maternal depression significantly predicted both internalizing and externalizing behaviors in linear regression models. Further, there was a significant interaction between maternal depression and treatment group, such that among mothers with higher depressive symptoms, the SB treatment attenuated the magnitude of the association between depression and child behavior. Findings suggest that while parenting support is important for all families, it may be particularly critical for those with higher levels of depression and underscores the need to consider multidimensional family processes in both research and clinical practice.

The functioning of the hypothalamic–pituitary–adrenal (HPA) axis is implicated in the etiology and maintenance of depressive and posttraumatic stress disorder (PTSD) symptoms. However, different maltreatment experiences as well as the increased sensitivity of the HPA axis during puberty may alter associations between the HPA axis and mental health. To address these gaps, the current study examined the potential bidirectional associations between cortisol reactivity to a stressor, PTSD symptoms, and depressive symptoms among early adolescents across two time points, 1 year apart (n = 454; Mage = 10.98 at Time 1 and Mage = 12.11 at Time 2). Multiple-group path models tested the pathways between cortiol reactivity and mental health prior to and during puberty, for different types of maltreatment . Overall, the results showed that associations between cortisol output and symptoms of PTSD and depression were driven by those in the midst of puberty. Specifically, higher cortisol output at Time 1 was linked with higher levels of subsequent PTSD and depressive symptoms for neglected youth who had reached puberty. However, depressive symptoms predicted subsequent lower cortisol output for the physical abuse and emotional abuse groups. These findings demonstrate longitudinal links between cortisol, depressive symptoms, and PTSD symptoms among youth with different types of maltreatment histories and highlight the need to consider the reorganization of the stress system during puberty in order to advance our understanding of the HPA axis and mental health.

Childhood anxiety disorders (CAD) are a common childhood mental disorder and understanding early developmental pathways is key to prevention and early intervention. What is not understood is whether early life stress predictors of CAD might be both mediated by infant cortisol reactivity and moderated by infant attachment status. To address this question, this exploratory study draws on 190 women recruited in early pregnancy and followed together with their children until 4 years of age. Early life stress is operationalized as maternal depression measured using the Structured Clinical Interview for the DSM, Childhood Trauma Questionnaire, Parenting Stress Index, and antenatal maternal hair cortisol concentrations. Infant cortisol reactivity was measured at 12 months together with the Strange Situation Procedure and CAD assessed at 4 years of age using the Preschool Age Psychiatric Assessment. There was no direct association between attachment classification and CAD. Furthermore, infant cortisol reactivity neither mediated nor attachment moderated the association of early life stress predictors and CAD. However, only for infants with organized attachment classifications, higher maternal antenatal depression, and hair cortisol were associated with a higher risk of CAD.

Research on marital quality and child well-being is currently limited by its common use of geographically constrained, homogenous, and often cross-sectional (or at least temporally limited) samples. We build upon previous work showing multiple trajectories of marital quality and data from the National Longitudinal Survey of Youth-1979 (NLSY79) regarding mothers and their children (inclusive of ages 5–14). We examine how indicators of child well-being are linked to parental trajectories of marital quality (happiness, communication, and conflict). Results showed children whose parents had consistently poor marital quality over the life course exhibited more internalizing and externalizing problems, poorer health, lower quality home environments, and lower math and vocabulary scores than children of parents in consistently higher-quality marriages. Group differences remained stable over time for child health, home environment, and vocabulary scores. Group differences for internalizing problems declined over time, whereas group differences increased for externalizing problems and math scores. Initial advantages for females across nearly all indicators of child well-being tended to shrink over time, with boys often moving slightly ahead by mid adolescence. We discuss the implications of these findings in regard to children's development and well-being and suggest treating marriage as a monolithic construct betrays important variation within marriage itself.

COVID-19 changed the landscape of employment and financial security in the USA, contributing to multi-systemic disruptions in family life. Using dyadic, daily-diary parent–adolescent data from a nationwide American sample (18,415 daily assessments; 29 days: 4/8/2020–4/21/2020 and 5/18/2020–6/1/2020; N = 635 parent–adolescent dyads), this intensive longitudinal study investigated how COVID-19-related job loss and working-from-home (WFH) arrangements influenced parents’ and children’s daily affect indirectly through family functioning (i.e., parent–adolescent conflict, inter-adult conflict, and parental warmth) and whether these links varied by family socioeconomic status (SES). Parental employment status was linked to these family relational dynamics, which were then connected to parents’ and adolescents’ daily affect. Although SES did not moderate these links, low-income families were more likely to experience job loss, parent–adolescent conflict, and inter-adult conflict and less likely to WFH than higher-income families. As inter-relations within the family are a malleable point for intervention, clinicians working with families recovering from the fiscal impact of the COVID-19 pandemic are encouraged to use approaches that strengthen family relationships, especially between adolescents and their parents. Unemployment subsidies are discussed as a means to support families struggling with job loss, and organizations are urged to consider the benefits of WFH on employee health and work-life balance.

We examined the associations of middle childhood and adolescence nighttime sleep duration with adolescence internalizing and externalizing behavior problems per the Youth Self-Report (YSR) and the Child Behavior Checklist (CBCL) questionnaires, in a cohort of 889 Colombian schoolchildren. We estimated adjusted differences with 95% confidence intervals (CI) in mean behavior problem t-scores in standardized units between recommended sleep duration categories and as a continuous exposure using multiple linear regression and restricted cubic spline models, respectively. Compared with sleep duration within recommendations, middle childhood sleep above recommendations was related to 4.6 (95% CI: 1.6, 7.6; p = .004) and 5.4 (95% CI: 1.2, 9.7; p = .01) adjusted units higher YSR and CBCL externalizing problem scores, respectively. In continuous exposure analyses, this association seemed restricted to children aged ≥11 years. Longer sleep, both in categories and as a continuous exposure, was also associated with increased CBCL internalizing problems. Results did not differ by sex or weekend/weekday sleep. Sleeping under recommendations in middle childhood was not significantly related to behavior problems; nevertheless, shorter sleep in adolescence, in both categorical and continuous scales, was significantly related to behavior problems. In conclusion, behavior problems in adolescence are associated with longer sleep in middle childhood and shorter sleep in adolescence.

This reflection on the history and future of developmental resilience science (DRS) highlights its co-emergence with developmental psychopathology (DP), as well as the roles of this journal and its founding editor, Dante Cicchetti, in the evolution of these intertwined domains of scholarship. A remarkable constellation of scholars at the University of Minnesota shaped the course of both conceptual frameworks and their dissemination. I describe fundamental assumptions common to DP and DRS frameworks that reflect their common roots and the pervasive influence of systems theory on developmental science. I describe four waves of DRS and key principles of DRS at the present time. In conclusion, I consider the possibility that a fifth wave of DRS is emerging with a focus on understanding patterns of multisystem, multilevel processes of resilience and their implications for interventions in the context of interacting, interdependent, and complex adaptive systems. I close this commentary with questions for future research and a hopeful outlook on the future of human resilience.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype–environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype–environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

Effects of stresses associated with extremely preterm birth may be biologically “recorded” in the genomes of individuals born preterm via changes in DNA methylation (DNAm) patterns. Genome-wide DNAm profiles were examined in buccal epithelial cells from 45 adults born at extremely low birth weight (ELBW; ≤1000 g) in the oldest known cohort of prospectively followed ELBW survivors (Mage = 32.35 years, 17 male), and 47 normal birth weight (NBW; ≥2500 g) control adults (Mage = 32.43 years, 20 male). Sex differences in DNAm profiles were found in both birth weight groups, but they were greatly enhanced in the ELBW group (77,895 loci) versus the NBW group (3,424 loci), suggesting synergistic effects of extreme prenatal adversity and sex on adult DNAm profiles. In men, DNAm profiles differed by birth weight group at 1,354 loci on 694 unique genes. Only two loci on two genes distinguished between ELBW and NBW women. Gene ontology (GO) and network analyses indicated that loci differentiating between ELBW and NBW men were abundant in genes within biological pathways related to neuronal development, synaptic transportation, metabolic regulation, and cellular regulation. Findings suggest increased sensitivity of males to long-term epigenetic effects of extremely preterm birth. Group differences are discussed in relation to particular gene functions.

Differential susceptibility theory (DST) posits that individuals differ in their developmental plasticity: some children are highly responsive to both environmental adversity and support, while others are less affected. According to this theory, “plasticity” genes that confer risk for psychopathology in adverse environments may promote superior functioning in supportive environments. We tested DST using a broad measure of child genetic liability (based on birth parent psychopathology), adoptive home environmental variables (e.g., marital warmth, parenting stress, and internalizing symptoms), and measures of child externalizing problems (n = 337) and social competence (n = 330) in 54-month-old adopted children from the Early Growth and Development Study. This adoption design is useful for examining DST because children are placed at birth or shortly thereafter with nongenetically related adoptive parents, naturally disentangling heritable and postnatal environmental effects. We conducted a series of multivariable regression analyses that included Gene × Environment interaction terms and found little evidence of DST; rather, interactions varied depending on the environmental factor of interest, in both significance and shape. Our mixed findings suggest further investigation of DST is warranted before tailoring screening and intervention recommendations to children based on their genetic liability or “sensitivity.”

The recent introduction of the induced pluripotent stem cell technology has made possible the derivation of neuronal cells from somatic cells obtained from human individuals. This in turn has opened new areas of investigation that can potentially bridge the gap between neuroscience and psychopathology. For the first time we can study the cell biology and genetics of neurons derived from any individual. Furthermore, by recapitulating in vitro the developmental steps whereby stem cells give rise to neuronal cells, we can now hope to understand factors that control typical and atypical development. We can begin to explore how human genes and their variants are transcribed into messenger RNAs within developing neurons and how these gene transcripts control the biology of developing cells. Thus, human-induced pluripotent stem cells have the potential to uncover not only what aspects of development are uniquely human but also variations in the series of events necessary for normal human brain development that predispose to psychopathology.

Gene-environment correlations and interactions for the relationship between emotional problems (EP) and family environment in adolescents in low- to middle-income countries (LMIC) have been rarely investigated. In total, 3207 adolescent twins aged 12–18 (Mean = 14.6 ± 1.73) years attending public schools in Lagos State in Nigeria completed measures of EP and Family Chaos (FC). Model-fitting analyses suggested that genetic and non-shared environmental influences on EP were 21% and 71%, respectively, and the corresponding estimates were 23% and 71% for FC. Shared environmental influences were not significant (8% and 6% respectively). Phenotypic correlation between EP and FC was .30 (95% CI = .27–.34), which was significantly influenced by genetic (A – 49%, 95% CI: 0.01–0.97) and non-shared environmental factors (E – 32%, 95% CI: 0.10–0.54). Shared environmental influences were not significant (C – 19%, 95% CI: −0.13 to 0.50). Moderation effects were significant whereby as FC increased, A on EP decreased (βA = −0.07, 95% CI: −0.12 to −0.02) while E increased (βE = 0.06, 95% CI: 0.03–0.09). Our findings indicate that genetic and non-shared environmental risk factors may mediate the relationship between EP and FC, and that as FC increases, protective genetic influences on EP may be attenuated, whereas environmental influences may become stronger in adolescents in LMIC.

Autism spectrum disorder (ASD) is heterogeneous and likely entails distinct phenotypes with varying etiologies. Identifying these subgroups may contribute to hypotheses about differential treatment responses. The present study aimed to discern subgroups among children with ASD and anxiety in context of the five-factor model of personality (FFM) and evaluate treatment response differences to two cognitive-behavioral therapy treatments. The present study is a secondary data analysis of children with ASD and anxiety (N=202; ages 7–13; 20.8% female) in a cognitive behavioral therapy (CBT) randomized controlled trial (Wood et al., 2020). Subgroups were identified via latent profile analysis of parent-reported FFM data. Treatment groups included standard-of-practice CBT (CC), designed for children with anxiety, and adapted CBT (BIACA), designed for children with ASD and comorbid anxiety. Five subgroups with distinct profiles were extracted. Analysis of covariance revealed CBT response was contingent on subgroup membership. Two subgroups responded better to BIACA on the primary outcome measure and a third responded better to BIACA on a peer-social adaptation measure, while a fourth subgroup responded better to CC on a school-related adaptation measure. These findings suggest that the FFM may be useful in empirically identifying subgroups of children with ASD, which could inform intervention selection decisions for children with ASD and anxiety.

Developmental psychopathology started as an intersection of fields and is now a field itself. As we contemplate the future of this field, we consider the ways in which a newer, interdisciplinary field – human developmental neuroscience – can inform, and be informed by, developmental psychopathology. To do so, we outline principles of developmental psychopathology and how they are and/or can be implemented in developmental neuroscience. In turn, we highlight how the collaboration between these fields can lead to richer models and more impactful translation. In doing so, we describe the ways in which models from developmental psychopathology can enrich developmental neuroscience and future directions for developmental psychopathology.

An enduring issue in the study of mental health is identifying developmental processes that explain how childhood characteristics progress to maladaptive forms. We examine the role that behavioral inhibition (BI) has on social anxiety (SA) during adolescence in 868 families of twins assessed at ages 8, 13, and 15 years. Multimodal assessments of BI and SA were completed at each phase, with additional measures (e.g., parenting stress) for parents and twins. Analyses were conducted in several steps: first, we used a cross-lagged panel model to demonstrate bidirectional paths between BI and SA; second a biometric Cholesky decomposition showed that both genetic and environmental influences on childhood BI also affect adolescent SA; next, multilevel phenotypic models tested moderation effects between BI and SA. We tested seven potential moderators of the BI to SA prediction in individual models and included only those that emerged as significant in a final conditional model examining predictors of SA. Though several main effects emerged as significant, only parenting stress had a significant interaction with BI to predict SA, highlighting the importance of environmental moderators in models examining temperamental effects on later psychological symptoms. This comprehensive assessment continues to build the prototype for such developmental psychopathology models.