Summary The frontal lobes control wide-ranging cognitive functions; however, functional subdivisions of human frontal cortex are only coarsely mapped. Here, functional magnetic resonance imaging reveals two distinct visual-biased attention regions in lateral frontal cortex, superior precentral sulcus (sPCS) and inferior precentral sulcus (iPCS), anatomically interdigitated with two auditory-biased attention regions, transverse gyrus intersecting precentral sulcus (tgPCS) and caudal inferior frontal sulcus (cIFS). Intrinsic functional connectivity analysis demonstrates that sPCS and iPCS fall within a broad visual-attention network, while tgPCS and cIFS fall within a broad auditory-attention network. Interestingly, we observe that spatial and temporal short-term memory (STM), respectively, recruit visual and auditory attention networks in the frontal lobe, independent of sensory modality. These findings not only demonstrate that both sensory modality and information domain influence frontal lobe functional organization, they also demonstrate that spatial processing co-localizes with visual processing and that temporal processing co-localizes with auditory processing in lateral frontal cortex.

Life history theory argues that exposure to early life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 54 studies (n ϭ 116,010) examining associations of ELA with pubertal timing and cellular aging (telomere length and DNA methylation age), systematically review 25 studies (n ϭ 3,253) examining ELA and neural markers of accelerated development (cortical thickness and amygdala-prefrontal cortex functional connectivity) and evaluate whether associations of ELA with biological aging vary according to the nature of adversity experienced. ELA overall was associated with accelerated pubertal timing (d ϭ Ϫ0.10) and cellular aging (d ϭ Ϫ0.21), but these associations varied by adversity type. Moderator analysis revealed that ELA characterized by threat was associated with accelerated pubertal development (d ϭ Ϫ0.26) and accelerated cellular aging (d ϭ Ϫ0.43), but deprivation and SES were unrelated to accelerated development. Systematic review revealed associations between ELA and accelerated cortical thinning, with threatrelated ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks. There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention. Public Significance StatementThis meta-analysis and systematic review suggests that biological aging following early life adversity, including earlier pubertal timing, advanced cellular aging, and accelerated thinning of the cortex, may be specific to children and adolescents who experienced violent or traumatic experiences early in childhood. No such effect was found for children who experienced deprivation or poverty in the absence of violence or trauma. These findings highlight a potential role of accelerated biological aging in health disparities associated with early life trauma, and a potential target for early interventions.

Growing evidence suggests that childhood socioeconomic status (SES) influences neural development, which may contribute to the well-documented SES-related disparities in academic achievement. However, the particular aspects of SES that impact neural structure and function are not well understood. Here, we investigate associations of childhood SES and a potential mechanism-degree of cognitive stimulation in the home environment-with cortical structure, white matter microstructure, and neural function during a working memory (WM) task across development. Analyses included 53 youths (age 6-19 years). Higher SES as reflected in the income-to-needs ratio was associated with higher parent-reported achievement, WM performance, and cognitive stimulation in the home environment. Although SES was not significantly associated with cortical thickness, children raised in more cognitively stimulating environments had thicker cortex in the frontoparietal network and cognitive stimulation mediated the assocation between SES and cortical thickness in the frontoparietal network. Higher family SES was associated with white matter microstructure and neural activation in the frontoparietal network during a WM task, including greater fractional anisotropy (FA) in the right and left superior longitudinal fasciculi (SLF), and greater BOLD activation in multiple regions of the prefrontal cortex during WM encoding and maintenance. Greater FA and activation in these regions was associated higher parent-reported achievement. Together, cognitive stimulation, WM performance, FA in the SLF, and prefrontal activation during WM encoding and maintenance significantly mediated the association between SES and parent-reported achievement. These findings highlight potential neural, cognitive, and environmental mechanisms linking SES with academic achievement and suggest that enhancing cognitive stimulation in the home environment might be one effective strategy for reducing SES-related disparities in academic outcomes.

Executive functions (EF), including working memory, inhibition, and cognitive flexibility, vary as a function of socioeconomic status (SES), with children from economically disadvantaged backgrounds having poorer performance than their higher SES peers. Using observational methods, we investigated cognitive stimulation in the home as a mechanism linking SES with EF. In a sample of 101 children aged 60–75 months, cognitive stimulation fully mediated SES‐related differences in EF. Critically, cognitive stimulation was positively associated with the development of inhibition and cognitive flexibility across an 18‐month follow‐up period. Furthermore, EF at T1 explained SES‐related differences in academic achievement at T2. Early cognitive stimulation—a modifiable factor—may be a desirable target for interventions designed to ameliorate SES‐related differences in cognitive development and academic achievement.

Childhood adversity is associated with altered reward processing, but little is known about whether this varies across distinct types of adversity. In a sample of 94 children (6-19 years), we investigated whether experiences of material deprivation, emotional deprivation, and trauma have differential associations with reward-related behavior and white matter microstructure in tracts involved in reward processing. Material deprivation (food insecurity), but not emotional deprivation or trauma, was associated with poor reward performance. Adversity-related influences on the integrity of white matter microstructure in frontostriatal tracts varied across childhood adversity types, and reductions in frontostriatal white matter integrity mediated the association of food insecurity with depressive symptoms. These findings document distinct behavioral and neurodevelopmental consequences of specific forms of adversity that have implications for psychopathology risk.

Childhood maltreatment is strongly associated with depression, which is characterized by reduced reactivity to reward. Identifying factors that mitigate risk for depression in maltreated children is important for understanding etiological links between maltreatment and depression as well as improving early intervention and prevention. We examine whether high reward reactivity at behavioral and neurobiological levels is a marker of resilience to depressive symptomology in adolescence following childhood maltreatment. A sample of 59 adolescents (21 with a history of maltreatment; Mean Age=16.95 years, SD =1.44) completed an fMRI task involving passive viewing of emotional stimuli. BOLD signal changes to positive relative to neutral images were extracted in basal ganglia regions of interest. Participants also completed a behavioral reward-processing task outside the scanner. Depression symptoms were assessed at the time of the MRI and again two years later. Greater reward reactivity across behavioral and neurobiological measures moderated the association of maltreatment with baseline depression. Specifically, faster reaction time to cues paired with monetary reward relative to those unpaired with reward and greater BOLD signal in the left pallidum was associated with lower depression symptoms in maltreated youth. Longitudinally, greater BOLD signal in the left putamen moderated change in depression scores over time, such that higher levels of reward response were associated with lower increases in depression over time among maltreated youths. Reactivity to monetary reward and positive social images, at both behavioral and neurobiological levels, is a potential marker of resilience to depression among adolescents exposed to maltreatment. These findings add to a growing body of work highlighting individual differences in reactivity to reward as a core neurodevelopmental mechanism in the etiology of depression.

Life history theory argues that exposure to early-life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 46 studies (n=64,925) examining associations of ELA with pubertal timing and cellular aging (telomere length and DNA methylation age), systematically review 19 studies (n=2276) examining ELA and neural markers of accelerated development (cortical thickness and amygdala-prefrontal cortex functional connectivity) and evaluate whether associations of ELA with biological aging vary according to the nature of adversity experienced. ELA overall was associated with accelerated pubertal timing (d=-0.12) and cellular aging (d=-0.32). Moderator analysis revealed that ELA characterized by threat (d=-0.26), but not deprivation or SES, was associated with accelerated pubertal development. Similarly, exposure to threat-related ELA was associated with accelerated cellular aging (d=-0.43), but not deprivation or SES.Systematic review revealed associations between ELA and accelerated cortical thinning, with threat-related ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks.There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention.

The COVID-19 pandemic has introduced novel stressors into the lives of youth. Identifying factors that protect against the onset of psychopathology in the face of these stressors is critical. We examine a wide range of factors that may protect youth from developing psychopathology during the pandemic. We assessed pandemic-related stressors, internalizing and externalizing psychopathology, and potential protective factors by combining two longitudinal samples of children and adolescents (N = 224, 7–10 and 13–15 years) assessed prior to the pandemic, during the stay-at-home orders, and six months later. We evaluated how family behaviors during the stay-at-home orders were related to changes in psychopathology during the pandemic, identified factors that moderate the association of pandemic-related stressors with psychopathology, and determined whether associations varied by age. Internalizing and externalizing psychopathology increased substantially during the pandemic. Higher exposure to pandemic-related stressors was associated with increases in internalizing and externalizing symptoms early in the pandemic and six months later. Having a structured routine, less passive screen time, lower exposure to news media about the pandemic, and to a lesser extent more time in nature and getting adequate sleep were associated with reduced psychopathology. The association between pandemic-related stressors and psychopathology was reduced for youths with limited passive screen time and was absent for children, but not adolescents, with lower news media consumption related to the pandemic. We provide insight into simple, practical steps families can take to promote resilience against mental health problems in youth during the COVID-19 pandemic and protect against psychopathology following pandemic-related stressors.