A Developmental Perspective on Early and Current Motor Abnormalities and Psychotic-Like Symptoms.

BACKGROUND AND HYPOTHESIS: Psychotic-like experiences (PLEs) are prevalent in the general population and, because they represent a lower end of the psychosis vulnerability spectrum, may be useful in informing mechanistic understanding. Although it is well-understood that motor signs characterize formal psychotic disorders, the developmental trajectory of these features and their relationships with PLEs are less well-understood. STUDY DESIGN: Data from 7559 adolescents and young adults (age 11-21) in the Philadelphia Neurodevelopmental Cohort were used to investigate whether early-life milestone-attainment delays relate to current adolescent sensorimotor functioning and positive and negative PLEs. Current sensorimotor functioning was assessed using the Computerized Finger Tapping task (assessing motor slowing) and Mouse Practice task (assessing sensorimotor planning). STUDY RESULTS: Early developmental abnormalities were related to current adolescent-aged motor slowing (t(7415.3) = -7.74, corrected-P < .001) and impaired sensorimotor planning (t(7502.5) = 5.57, corrected-P < .001). There was a significant interaction between developmental delays and current sensorimotor functioning on positive and negative PLEs (t = 1.67-4.51), such that individuals with early developmental delays had a stronger positive relationship between sensorimotor dysfunction and PLEs. Importantly, interaction models were significantly better at explaining current PLEs than those treating early and current sensorimotor dysfunction independently (χ2 = 4.89-20.34). CONCLUSIONS: These findings suggest a relationship between early developmental delays and current sensorimotor functioning in psychosis proneness and inform an understanding of heterotypic continuity as well as a neurodevelopmental perspective of motor circuits. Furthermore, results indicate that motor signs are a clear factor in the psychosis continuum, suggesting that they may represent a core feature of psychosis vulnerability.

Developmental changes in the endorsement of psychotic-like experiences from middle childhood through young adulthood.

BACKGROUND: Children tend to endorse psychotic-like experiences (PLEs) at higher rates than adults, although little is known about how specific symptom endorsement changes across the span of development. Here we take an observational approach to examine trends in PLE endorsement by age in two non-clinical samples: one of school-aged children and another of late adolescents and early adults. METHODS: Prodromal Questionnaire-Brief (child and adult versions) responses were investigated in individuals ages 9-13 (n = 11865) and 16-24 (n = 3209) from the Adolescent Brain and Cognitive Development Study (ABCD) and the Multisite Assessment of Psychosis-risk Study (MAP), respectively. Item-level endorsement and distressing item frequencies were examined by age throughout both cohorts. RESULTS: Unusual perceptual experiences were generally endorsed more heavily in childhood, while other PLEs were endorsed in adolescents and adults up to 4.8 times more frequently than in children. Additionally, certain experiences were endorsed by as many as 73 percent of the older sample. CONCLUSIONS: Considerations for the measurement of PLEs in childhood and adolescence are underscored. Findings from these two samples provide a window into the course of these PLEs and may serve as a scaffold for future research investigating normative versus risk-related experiences during development.

Physical and mental health in adolescence: novel insights from a transdiagnostic examination of FitBit data in the ABCD study.

Adolescence is among the most vulnerable period for the emergence of serious mental illnesses. Addressing this vulnerability has generated interest in identifying markers of risk for symptoms and opportunities for early intervention. Physical fitness has been linked to psychopathology and may be a useful risk marker and target for early intervention. New wearable technology has made assessing fitness behavior more practical while avoiding recall and self-report bias. Still, questions remain regarding the clinical utility of physical fitness metrics for mental health, both transdiagnostically and along specific symptom dimensions. The current study includes 5007 adolescents (ages 10-13) who participated in the Adolescent Brain Cognitive Development (ABCD) study and additional sub-study that collected fitness data from wearable technology and clinical symptom measures. Physical fitness metrics included resting heart rate (RHR- an index of cardiovascular health), time spent sedentary (associated with increased inflammation and cardiovascular disease), and time spent in moderate physical activity (associated with increased neurogenesis, neuroplasticity, and healthy neurodevelopment). Self-report clinical symptoms included measures of psychosis-like experiences (PLE), internalizing symptoms, and externalizing symptoms. Increased RHR- lower cardiovascular fitness- related only to greater internalizing symptoms (t = 3.63). More sedentary behavior related to elevated PLE severity (t = 5.49). More moderate activity related to lower PLE (t = -2.69) and internalizing (t = -6.29) symptom severity. Wearable technology fitness metrics linked physical health to specific mental health dimensions, which emphasizes the utility of detailed digital health data as a marker for risk and the need for precision in targeting physical health behaviors to benefit symptoms of psychopathology.

Longitudinal study of peer victimization, social support, and mental health during early adolescence.

BACKGROUND: Peer victimization predicts the development of mental health symptoms in the transition to adolescence, but it is unclear whether and how parents and school environments can buffer this link. METHODS: We analyzed two-year longitudinal data from the Adolescent Brain Cognitive Development (ABCD) study, involving a diverse sample of 11 844 children across the United States (average at baseline = 9.91 years; standard deviation = 0.63; range = 8.92-11.08; complete case sample = 8385). Longitudinal associations between peer victimization and two-year changes in mental health symptoms of major depression disorder (MDD), separation anxiety (SA), prodromal psychosis (PP), and attention-deficit/hyperactivity disorder (ADHD) were examined including a wide range of covariates. Mixed linear models were used to test for the moderating effects of parental warmth and prosocial school environment. RESULTS: 20% of children experienced peer victimization. Higher exposure to peer victimization was associated with increases in MDD, SA, and ADHD symptoms. Parental warmth was associated with decreases in MDD symptoms but did not robustly buffer the link between peer victimization and mental health symptoms. Prosocial school environment predicted decreases in PP symptoms and buffered the link between peer victimization and MDD symptoms but amplified the link between peer victimization and SA and ADHD symptoms. CONCLUSIONS: Peer victimization is associated with increases in mental health symptoms during the transition to adolescence. Parental warmth and prosocial school environments might not be enough to counter the negative consequences of peer victimization on all mental health outcomes.

Physical and Mental Health in Adolescence: Novel Insights from a transdiagnostic examination of FitBit data in the ABCD Study.

Adolescence is among the most vulnerable period for the emergence of serious mental illnesses. Addressing this vulnerability has generated interest in identifying markers of risk for symptoms and opportunities for early intervention. Physical fitness has been linked to psychopathology and may be a useful risk marker and target for early intervention. New wearable technology has made assessing fitness behavior more practical while avoiding recall and self-report bias. Still, questions remain regarding the clinical utility of physical fitness metrics for mental health, both transdiagnostically and along specific symptom dimensions. The current study includes 5007 adolescents (ages 10 to 13) who participated in the Adolescent Brain Cognitive Development (ABCD) study and additional sub-study that collected fitness data from wearable technology and clinical symptom measures. Physical fitness metrics included resting heart rate (RHR- an index of cardiovascular health), time spent sedentary (associated with increased inflammation and cardiovascular disease), and time spent in moderate physical activity (associated with increased neurogenesis, neuroplasticity, and healthy neurodevelopment). Self-report clinical symptoms included measures of internalizing symptoms, externalizing symptoms, and psychosis-like experiences - PLE). Increased RHR- lower cardiovascular fitness- related only to greater internalizing symptoms (t = 3.63). More sedentary behavior related to elevated PLE severity (t = 5.49). More moderate activity related to lower PLE (t=-2.69) and internalizing (t=-6.29) symptom severity. Wearable technology fitness metrics linked physical health to specific mental health dimensions, which emphasizes the utility of detailed digital health data as a marker for risk and the need for precision in targeting physical health behaviors to benefit symptoms of psychopathology.

Neurodevelopmental vulnerability to psychosis: developmentally-based methods enable detection of early life inhibitory control deficits that predict psychotic-like experiences at the transition to adolescence.

BACKGROUND: Inhibitory control develops in early childhood, and atypical development may be a measurable marker of risk for the later development of psychosis. Additionally, inhibitory control may be a target for intervention. METHODS: Behavioral performance on a developmentally appropriate Go/No-Go task including a frustration manipulation completed by children ages 3-5 years (early childhood; n = 107) was examined in relation to psychotic-like experiences (PLEs; 'tween'; ages 9-12), internalizing symptoms, and externalizing symptoms self-reported at long-term follow-up (pre-adolescence; ages 8-11). ERP N200 amplitude for a subset of these children (n = 34) with electrophysiological data during the task was examined as an index of inhibitory control. RESULTS: Children with lower accuracy on No-Go trials compared to Go trials in early childhood (F(1,101) = 3.976, p = 0.049), evidenced higher PLEs at the transition to adolescence 4-9 years later, reflecting a specific deficit in inhibitory control. No association was observed with internalizing or externalizing symptoms. Decreased accuracy during the frustration manipulation predicted higher internalizing, F(2,202) = 5.618, p = 0.004, and externalizing symptoms, F(2,202) = 4.663, p = 0.010. Smaller N200 amplitudes were observed on No-Go trials for those with higher PLEs, F(1,101) = 6.075, p = 0.020; no relationship was observed for internalizing or externalizing symptoms. CONCLUSIONS: Long-term follow-up demonstrates for the first time a specific deficit in inhibitory control behaviorally and electrophysiology, for individuals who later report more PLEs. Decreases in task performance under frustration induction indicated risk for internalizing and externalizing symptoms. These findings suggest that pathophysiological mechanisms for psychosis are relevant and discriminable in early childhood, and further, suggest an identifiable and potentially modifiable target for early intervention.

Brain morphometry points to emerging patterns of psychosis, depression, and anxiety vulnerability over a 2-year period in childhood.

BACKGROUND: Gray matter morphometry studies have lent seminal insights into the etiology of mental illness. Existing research has primarily focused on adults and then, typically on a single disorder. Examining brain characteristics in late childhood, when the brain is preparing to undergo significant adolescent reorganization and various forms of serious psychopathology are just first emerging, may allow for a unique and highly important perspective of overlapping and unique pathogenesis. METHODS: A total of 8645 youth were recruited as part of the Adolescent Brain and Cognitive Development study. Magnetic resonance imaging scans were collected, and psychotic-like experiences (PLEs), depressive, and anxiety symptoms were assessed three times over a 2-year period. Cortical thickness, surface area, and subcortical volume were used to predict baseline symptomatology and symptom progression over time. RESULTS: Some features could possibly signal common vulnerability, predicting progression across forms of psychopathology (e.g. superior frontal and middle temporal regions). However, there was a specific predictive value for emerging PLEs (lateral occipital and precentral thickness), anxiety (parietal thickness/area and cingulate), and depression (e.g. parahippocampal and inferior temporal). CONCLUSION: Findings indicate common and distinct patterns of vulnerability for varying forms of psychopathology are present during late childhood, before the adolescent reorganization, and have direct relevance for informing novel conceptual models along with early prevention and intervention efforts.

Hippocampal subfields, daily stressors, and resting cortisol in individuals at clinical high-risk for psychosis.

INTRODUCTION: The hippocampus, comprised of functionally distinct subfields, both regulates stress and is affected by it during psychosis pathogenesis. Hippocampal abnormalities are evident across psychosis spectrum and are associated with aberrant cortisol levels and greater environmental stressors exposure. These associations, particularly at the subfield-level, are poorly understood in individuals at clinical high-risk (CHR) for psychosis. This represents a significant literature gap given this critical pathogenetic period is characterized by an interplay between environmental stressors and biological susceptibility. METHODS: A total of 121 participants including 51 CHR (mean age=18.61) and 70 healthy controls (HC; mean age=18.3) were enrolled in the study. Participants completed a structural scan, salivary cortisol assays, and a self-report measure assessing distress from daily stressors exposure (DSI). Hippocampal subfield segmentation was conducted using Freesurfer. RESULTS: Smaller hippocampal subfields were associated with greater stress levels. Greater DSI was associated with lower volumes in CA1 (r = -0.38) and CA2/3 (r = -0.29), but not in CA4/DG (r = -0.28), presubiculum (r = -0.09), or subiculum (r = -0.17). Higher resting cortisol was associated with lower volumes in presubiculum (r = -0.4) but not subiculum (r = -0.22), CA1 (r = 0.08), CA2/3 (r = 0.1), or CA4/DG (r = -0.005). Regressions indicated effects for CA1 and DSI (ß = 0.57, p = .03) and presubiculum and cortisol (ß = 0.61, p = .02) are specific to CHR participants relative to HCs. CONCLUSIONS: The findings provided insights into links between stress and brain vulnerability during psychosis-risk period. Regional differences highlighted potentially different mechanisms by which stress impacts specific subfields. Presubiculum may be more susceptible to the impact of early stress on HPA-axis and cornu amonis to acute stressors.

Depression and Psychosis Risk Shared Vulnerability for Motor Signs Across Development, Symptom Dimensions, and Familial Risk.

BACKGROUND: Motor abnormalities are strong transdiagnostic indicators of psychopathology risk that reflect emerging neural network abnormalities. Indeed, motor signs, such as motor slowing and agitation, are widely recognized as core features of both psychosis and depression. However, it is unclear whether these reflect shared or distinct etiology. METHODS: A sample of 11 878 adolescents completed self-reported clinical measures of rated psychotic-like experiences (PLEs) and depression. Familial risk for psychopathology and the presence of motor signs were drawn from parental reports, including developmental motor delays (eg, sitting, walking), and adolescent motor signs (eg, dyscoordination, psychomotor retardation, and psychomotor agitation). Finally, motor network connectivity in theoretically relevant networks (cortico-striatal, cortico-thalamic, and cortico-cerebellar) were related to symptoms and familial risk for psychopathology. RESULTS: Developmental motor delays related to increased PLEs, increased depression symptoms, and greater familial risk. Familial risk for both PLEs and depression showed higher rates of developmental motor delays than all other groups. Adolescent motor signs, however, showed unique patterns of relationships to symptoms and familial risk such that dyscoordination reflected risk for PLEs, both psychomotor agitation and retardation reflected depression risk, and psychomotor agitation reflected transdiagnostic risk. Cortico-striatal connectivity was related to depression and PLEs, but cortico-cerebellar connectivity was linked to PLEs only. CONCLUSIONS: Motor signs may be a transdiagnostic marker of vulnerability for psychopathology. Early developmental motor delays could belie pluripotent, familial risk features. Unique items, eg, dyscoordination specifically related to PLEs, possibly reflecting processes inherent in distinct emerging forms of psychopathology.

Differentiating kinds of systemic stressors with relation to psychotic-like experiences in late childhood and early adolescence: the stimulation, discrepancy, and deprivation model of psychosis.

INTRODUCTION: Conceptualizations that distinguish systems-level stress exposures are lacking; the Stimulation (lack of safety and high attentional demands), Discrepancy (social exclusion and lack of belonging), and Deprivation (lack of environmental enrichment) (SDD) theory of psychosis and stressors occurring at the systems-level has not been directly tested. METHODS: Exploratory factor analysis was conducted on 3,207 youth, and associations with psychotic-like experiences (PLEs) were explored. RESULTS: Though model fit was suboptimal, five factors were defined, and four were consistent with the SDD theory, and related to PLEs. Objective and subjective/self-report exposures for deprivation showed significantly stronger PLE associations compared to discrepancy and objective stimulation factors. Objective and subjective/self-report measures converged overall, though self-report stimulation exhibited a significantly stronger association with PLEs compared to objective stimulation. DISCUSSION: Considering distinct system-level exposures could help clarify putative mechanisms and psychosis vulnerability. The preliminary approach potentially informs health policy efforts aimed at psychopathology prevention and intervention.

Motor abnormalities, depression risk, and clinical course in adolescence.

Background: Motor abnormalities, such as psychomotor agitation and retardation, are widely recognized as core features of depression. However, it is not currently known if motor abnormalities connote risk for depression. Methods: Using data from the Adolescent Brain Cognitive Development (ABCD) Study, a nationally representative sample of youth (n=10,835, 9-11 years old), the present paper examines whether motor abnormalities are associated with (a) depression symptoms in early adolescence, (b) familial risk for depression (familial risk loading), and (c) future depression symptoms. Motor abnormalities measures included traditional (DSM) motor signs such as psychomotor agitation and retardation as well as other motor domains such as developmental motor delays and dyscoordination. Results: Traditional motor abnormalities were less prevalent (agitation=3.2%, retardation=0.3%) than non-traditional domains (delays=13.79%, coordination=35.5%) among adolescents. Motor dysfunction was associated with depression symptoms (Cohen's ds=0.02 to 0.12). Familial risk for depression was related to motor abnormalities (Cohen's ds=0.08 to 0.27), with the exception of motor retardation. Family vulnerability varied in sensitivity to depression risk (e.g., retardation: .53%; dyscoordination: 32.05%). Baseline endorsement of motor abnormalities predicted future depression symptoms at one-year follow-up. Conclusions: These findings suggest that motor signs reflect a novel, promising future direction for examining vulnerability to depression risk in early adolescence.

Neuropsychological Performance Among Individuals at Clinical High-Risk for Psychosis vs Putatively Low-Risk Peers With Other Psychopathology: A Systematic Review and Meta-Analysis.

BACKGROUND AND HYPOTHESIS: Youth at clinical high-risk (CHR) for psychosis present with neuropsychological impairments relative to healthy controls (HC), but whether these impairments are distinguishable from those seen among putatively lower risk peers with other psychopathology remains unknown. We hypothesized that any excess impairment among CHR cohorts beyond that seen in other clinical groups is minimal and accounted for by the proportion who transition to psychosis (CHR-T). STUDY DESIGN: We performed a systematic review and meta-analysis of studies comparing cognitive performance among CHR youth to clinical comparators (CC) who either sought mental health services but did not meet CHR criteria or presented with verified nonpsychotic psychopathology. STUDY RESULTS: Twenty-one studies were included representing nearly 4000 participants. Individuals at CHR showed substantial cognitive impairments relative to HC (eg, global cognition: g = -0.48 [-0.60, -0.34]), but minimal impairments relative to CC (eg, global cognition: g = -0.13 [-0.20, -0.06]). Any excess impairment among CHR was almost entirely attributable to CHR-T; impairment among youth at CHR without transition (CHR-NT) was typically indistinguishable from CC (eg, global cognition, CHR-T: g = -0.42 [-0.64, -0.19], CHR-NT: g = -0.09 [-0.18, 0.00]; processing speed, CHR-T: g = -0.59 [-0.82, -0.37], CHR-NT: g = -0.12 [-0.25, 0.07]; working memory, CHR-T: g = -0.42 [-0.62, -0.22], CHR-NT: g = -0.03 [-0.14, 0.08]). CONCLUSIONS: Neurocognitive impairment in CHR cohorts should be interpreted cautiously when psychosis or even CHR status is the specific clinical syndrome of interest as these impairments most likely represent a transdiagnostic vs psychosis-specific vulnerability.

Differentiating distinct and converging neural correlates of types of systemic environmental exposures.

Systemic environmental disadvantage relates to a host of health and functional outcomes. Specific structural factors have seldom been linked to neural structure, however, clouding understanding of putative mechanisms. Examining relations during childhood/preadolescence, a dynamic period of neurodevelopment, could aid bridge this gap. A total of 10,213 youth were recruited from the Adolescent Brain and Cognitive Development study. Self-report and objective measures (Census and Federal bureau of investigation metrics extracted using geocoding) of environmental exposures were used, including stimulation indexing lack of safety and high attentional demands, discrepancy indexing social exclusion/lack of belonging, and deprivation indexing lack of environmental enrichment. Environmental measures were related to cortical thickness, surface area, and subcortical volume regions, controlling for other environmental exposures and accounting for other brain regions. Self-report (|ß| = .04-.09) and objective (|ß| = .02-.06) environmental domains related to area/thickness in overlapping (e.g., insula, caudal anterior cingulate), and unique regions (e.g., for discrepancy, rostral anterior and isthmus cingulate, implicated in socioemotional functions; for stimulation, precuneus, critical for cue reactivity and integration of environmental cues; and for deprivation, superior frontal, integral to executive functioning). For stimulation and discrepancy exposures, self-report and objective measures showed similarities in correlate regions, while deprivation exposures evidenced distinct correlates for self-report and objective measures. Results represent a necessary step toward broader work aimed at establishing mechanisms and correlates of structural disadvantage, highlighting the relevance of going beyond aggregate models by considering types of environmental factors, and the need to incorporate both subjective and objective measurements in these efforts.

Genuine and non-genuine smiles in individuals meeting criteria for a clinical high-risk syndrome.

AIM: Psychosis is characterized by both alterations in emotional functioning and environmental stressors including bullying victimization. Recent evidence suggests that some alterations in emotional functioning (e.g., blunted positive facial expressions) are already present in the psychosis risk period. Yet, some clinically relevant facial emotions have not been investigated such as genuine smiles (thought to reflect genuine positive emotions) and non-genuine smiles (thought to fake positive or mask negative emotions) in individuals meeting criteria for a clinical high-risk (CHR) syndrome. Further, despite a compelling conceptual basis to suggest a link between affective expression and exposure to environmental stress, to date, no investigations have sought to examine this association. Here, we aim to assess differences between a sample of CHR (N = 65) and control (N = 67) individuals in genuine and non-genuine smiles and associations with bullying victimization. METHODS: Smiles (i.e., genuine; non-genuine) were objectively coded on a second-by-second basis using the Facial Action Coding System during a digitally recorded clinical interview segment. Bullying victimization was measured via parent report. RESULTS: Findings revealed that the CHR group (1) showed blunted genuine (but not non-genuine) smiles compared to controls. Moreover, (2) bullying victimization was related to blunted genuine smiles, but not non-genuine smiles. CONCLUSION: These findings expand our understanding of emotional alterations in this group with implications for diagnosis (highlighting blunted genuine smiles as a specific marker) and etiology (underscoring the role of bullying victimization in the etiology of emotional dysfunction).

Neuroimaging Markers of Resiliency in Youth at Clinical High Risk for Psychosis: A Qualitative Review.

Psychotic disorders are highly debilitating and constitute a major public health burden. Identifying markers of psychosis risk and resilience is a necessary step toward understanding etiology and informing prevention and treatment efforts in individuals at clinical high risk (CHR) for psychosis. In this context, it is important to consider that neural risk markers have been particularly useful in identifying mechanistic determinants along with predicting clinical outcomes. Notably, despite a growing body of supportive literature and the promise of recent findings identifying potential neural markers, the current work on CHR resilience markers has received little attention. The present review provides a brief overview of brain-based risk markers with a focus on predicting symptom course. Next, the review turns to protective markers, examining research from nonpsychiatric and schizophrenia fields to build an understanding of framing, priorities, and potential, applying these ideas to contextualizing a small but informative body of resiliency-relevant CHR research. Four domains (neurocognition, emotion regulation, allostatic load, and sensory and sensorimotor function) were identified and are discussed in terms of behavioral and neural markers. Taken together, the literature suggests significant predictive value for brain-based markers for individuals at CHR for psychosis, and the limited but compelling resiliency work highlights the critical importance of expanding this promising area of inquiry.

Translating RDoC to Real-World Impact in Developmental Psychopathology: A Neurodevelopmental Framework for Application of Mental Health Risk Calculators.

The National Institute of Mental Health Research Domain Criteria's (RDoC) has prompted a paradigm shift from categorical psychiatric disorders to considering multiple levels of vulnerability for probabilistic risk of disorder. However, the lack of neurodevelopmentally-based tools for clinical decision-making has limited RDoC's real-world impact. Integration with developmental psychopathology principles and statistical methods actualize the clinical implementation of RDoC to inform neurodevelopmental risk. In this conceptual paper, we introduce the probabilistic mental health risk calculator as an innovation for such translation and lay out a research agenda for generating an RDoC- and developmentally-informed paradigm that could be applied to predict a range of developmental psychopathologies from early childhood to young adulthood. We discuss methods that weigh the incremental utility for prediction based on intensity and burden of assessment, the addition of developmental change patterns, considerations for assessing outcomes, and integrative data approaches. Throughout, we illustrate the risk calculator approach with different neurodevelopmental pathways and phenotypes. Finally, we discuss real-world implementation of these methods for improving early identification and prevention of developmental psychopathology. We propose that mental health risk calculators can build a needed bridge between RDoC's multiple units of analysis and developmental science.

Psychotic-Like Experiences Associated with Sleep Disturbance and Brain Volumes in Youth: Findings from the Adolescent Brain Cognitive Development Study.

Background: Sleep disturbance is characteristic of schizophrenia and at-risk populations, suggesting a possible etiological role in psychosis. Biological mechanisms underlying associations between sleep and psychosis vulnerability are unclear, although reduced sleep-regulatory brain structure volumes are a proposed contributor. This study is the first to examine relationships between psychotic-like experiences (PLEs; subclinical symptoms reflecting psychosis vulnerability/risk), sleep, and brain volumes in youth. Methods: Brain volumes of five sleep-related structures were examined in relation to PLEs and difficulties initiating and maintaining sleep (DIMS) in 9260 9-11 year-olds participating in the Adolescent Brain Cognitive Development (ABCD) study. Analytic models examined relationships between DIMS, PLEs, and brain volumes, as well as DIMS as a mediator of brain volume-PLEs relationships. Although sleep regulation structures (i.e., thalamus, basal forebrain, hypothalamus) were of primary interest, other potentially-relevant structures to sleep-related functioning and psychosis (i.e., hippocampus, amygdala) were also examined. Results: PLEs were associated with increased DIMS as well as reduced volume in some, but not all, brain structures, including the thalamus and basal forebrain in children. DIMS was also associated with reduced left thalamus volume in youth. Increased DIMS partially, statistically mediated the relationship between left thalamic volume and PLEs, although the effect was relatively small. Conclusions: Results highlight left thalamic volume as a potential neural mechanism underlying sleep disturbances and PLEs in childhood. Future studies should assess causal relationships between sleep, PLEs, and brain structure across adolescent development, interactions with other psychosis risk factors, and the role of sleep interventions in prevention of psychosis and a range of psychiatric conditions across the lifespan.

Adaptability and cohesion in youth at clinical high-risk for psychosis: A multi-informant approach.

BACKGROUND: Families can play a critical role in the development of psychosis. Adaptability (i.e., flexibility) and cohesion (i.e., emotional bonding) are important markers of family functioning, but have rarely been studied in youth at clinical high risk for developing psychosis (CHR), especially not from a multi-informant perspective. METHODS: The current study examined adaptability and cohesion (using youth and mother reports) and clinical symptoms (in youth) among 75 youth at CHR and their mothers (N = 48) and 79 matched healthy controls and their mothers (N = 42). RESULTS: Findings showed that (1) youth at CHR and their mothers reported lower adaptability and cohesion than their healthy control counterparts. (2) All youth reported lower adaptability than mothers, but only youth at CHR (not control youth) reported lower cohesion than their mothers. (3) There were no significant links between CHR youth and mother reports of adaptability and cohesion and clinical symptoms. CONCLUSIONS: Findings support existing literature that families with a youth at CHR are at risk for poorer functioning and demonstrate pronounced youth-mother discrepancies with youth at CHR (but not controls) reporting lower emotional bonding than their mothers. Future studies may further probe multi-informant perspectives of family environment as a clinical marker in the clinical high risk state.

Neighborhood deprivation, prefrontal morphology and neurocognition in late childhood to early adolescence.

BACKGROUND: Neighborhood deprivation adversely effects neurodevelopment and cognitive function; however, mechanisms remain unexplored. Neighborhood deprivation could be particularly impactful in late childhood/early adolescence, in neural regions with protracted developmental trajectories, e.g., prefrontal cortex (PFC). METHODS: The Adolescent Brain Cognitive Development (ABCD) study recruited 10,205 youth. Geocoded residential history was used to extract individual neighborhood characteristics. A general cognitive ability index and MRI scans were completed. Associations with neurocognition were examined. The relation of PFC surface area and cortical thickness to neighborhood deprivation was tested. PFC subregions and asymmetry, with putative differential environmental susceptibility during key developmental periods, were explored. Analyses tested PFC area as a possible mediating mechanism. RESULTS: Neighborhood deprivation predicted neurocognitive performance (ߠ​= â€‹-0.11), even after accounting for parental education and household income (ߠ​= â€‹-0.07). Higher neighborhood deprivation related to greater overall PFC surface area (ηp2 â€‹= â€‹0.003), and differences in leftward asymmetry were observed for area (ηp2 â€‹= â€‹0.001), and thickness (ηp2 â€‹= â€‹0.003). Subregion analyses highlighted differences among critical areas that are actively developing in late childhood/early adolescence and are essential to modulating high order cognitive function. These included orbitofrontal, superior frontal, rostral middle frontal, and frontal pole regions (Cohen's d â€‹= â€‹0.03-0.09). PFC surface area partially mediated the relation between neighborhood deprivation and neurocognition. DISCUSSION: Neighborhood deprivation related to cognitive function (a foundational skill tied to a range of lifetime outcomes) and PFC morphology, with evidence found for partial mediation of PFC on neurocognitive function. Results inform public health conceptualizations of development and environmental vulnerability.