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 ( β = −0.11), even after accounting for parental education and household income ( β = −0.07). Higher neighborhood deprivation related to greater overall PFC surface area ( η 2 p = 0.003), and differences in leftward asymmetry were observed for area ( η 2 p = 0.001), and thickness ( η 2 p = 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 = 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.

Background Characterizing the link between childhood trauma and adult neurocognitive function in psychosis is crucial for improving the fields understanding of how early environmental risk factors impact the presentation of the disorder. To date, the literature has been inconsistent: meta-analytic synthesis is lacking, and it is unclear whether specific cognitive functions are affected. Methods A meta-analysis was performed on a total of 3315 subjects with a psychotic disorder. The links between childhood trauma, overall neurocognitive function, and four cognitive subdomains (working memory, executive function, verbal/visual memory, and attention/processing speed) were examined. Relevant sample characteristics and methodological moderators were tested. The strength of the association between trauma and overall neurocognition in individuals with psychotic disorders was also compared to that of healthy controls. Results Among individuals with psychotic disorders, there was a significant association between overall cognition and childhood trauma, r = −.055; 95% CI = −0.09, −0.02, P = .002. There was also a modest, negative relationship between childhood trauma and working memory, r = −.091; 95% CI = −0.15, −0.03, P = .002. Moderators did not have a significant effect on these analyses. Further, the association between childhood trauma and neurocognition was significantly stronger in healthy controls compared to patients with a psychotic disorder. Conclusion A small negative association was found between overall cognition and childhood trauma in individuals with psychotic disorders. Results suggest the association is less strong for individuals with a psychotic disorder compared to healthy populations. Findings are informative for prominent etiological models of psychosis.

Opinion Statement Schizophrenia is a devastating mental illness that has profound effects on a person’s health and quality of life. Exercise represents a promising new treatment option that may supplement current psychosocial and pharmacological interventions for psychosis. A large body of work suggests that exercise can improve cardio-metabolic and health behavior and facilitate neurogenesis in areas of the brain that are notably impacted by psychosis. Recent efforts to incorporate exercise as either stand-alone or adjunctive treatment for individuals with schizophrenia range from yoga and light stretching to moderately intense walking, bike riding, or team sports. These interventions suggest that moderately intense exercise may be beneficial for improving both positive and negative symptomatology, cognition and functioning. Indeed, exercise may be beneficial for decreasing risk factors for a wide range of health problems often observed in patients with schizophrenia, including weight gain and metabolic syndrome as well as tobacco and substance use. Given the positive results from interventions in schizophrenia patients, there is an impetus for incorporating exercise in the early stages of the disorder. Notably, individuals at ultrahigh risk (UHR) for psychosis report more sedentary behavior and perceive less benefit from exercise; interventions prior to the onset of the disorder may be helpful for increasing health behaviors, perhaps delaying or preventing the onset of psychosis. Taken together, for individuals with psychosis, exercise may provide holistic benefits for the neural to the social impairments.

Our study examined hippocampal subregion volumes cross-sectionally in a large sample across the psychosis spectrum, as well as links with hippocampus-mediated cognitive function. Our findings suggest that hippocampal abnormalities emerge before first psychosis episode onset, and may be etiologically informative.

Chronic stress exposure has been established as a key vulnerability factor for developing psychotic disorders, including schizophrenia. A structural, or systems level perspective, has often been lacking in conceptualizations of chronic stress for psychotic disorders. The current review thus identified three subtypes of structural exposures. Stimulation exposures included urban environments, population density and crime exposure, with intermediary mechanisms of lack of safety and high attentional demands. Underlying neural mechanisms included threat neural circuits. Discrepancy exposures included environmental ethnic density, income inequality, and social fragmentation, with intermediary mechanisms of lack of belonging and social exclusion, and neural mechanisms including the oxytocin system. Deprivation exposures included environments lacking socioeconomic, educational, or material resources, with intermediary mechanisms of lack of needed environmental enrichment, and underlying neural mechanisms of over-pruning and protracted PFC development. Delineating stressor etiology at the systems level is a necessary step in reducing barriers to effective interventions and health policy.