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Sowell, E. R.

Publications and source records attributed to Sowell, E. R..

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Longitudinal mapping of cortical change during early adolescence associated with prenatal tobacco and/or alcohol exposure in the Adolescent Brain Cognitive DevelopmentSM Study

ImportanceThe effects of prenatal alcohol (PAE) and tobacco exposure (PTE) on adolescent neuroanatomical development are typically evaluated cross-sectionally. It is unclear if observed effects persist throughout life or reflect different developmental trajectories. ObjectiveTo determine how PAE and PTE are associated with cortical structure and development across two timepoints in early adolescence. DesignObservational, longitudinal analyses of data within the Adolescent Brain Cognitive Development{square} Study Setting21 study sites in the United States Participants5,417 youth participants, aged [~]9-12 years old ExposuresPAE and PTE based on caregiver (self) reports of alcohol/tobacco use during pregnancy, before and after pregnancy recognition. Main Outcomes and MeasuresCortical thickness (mm) and cortical surface area (mm2) measured approximately 2 years apart in early adolescence, across 68 bilateral cortical regions. ResultsAt baseline data collection, youth participants were [~]9.9 years old (SD=0.6). At the second neuroimaging appointment, youth participants were [~]11.9 years old (SD=0.6). When modelling cortical thickness, we controlled for individuals whole-brain volume; when modelling cortical surface area, individuals total surface area. Cortical thickness generally declined with age. Cortical surface area either expanded or contracted with age, depending on region. PAE had minimal effects on cortical structure (main effects) and development (PAExAge interactions). PTE had robust effects on cortical thickness and was associated with faster rates of cortical thinning in several regions within the frontal lobe. Post hoc analyses on (1) the effects of PTE for those who continued tobacco use after pregnancy recognition and (2) the effects of PTE in those who did not also use alcohol revealed weaker effects. Conclusions and RelevancePTE had robust effects on neuroanatomical structure and longitudinal development, particularly cortical thickness. Analyzing developmental cortical trajectories informs how PTE and/or PAE not only affects cortical structure but how it develops long after those prenatal exposures occurred. Future analyses involving cotinine biomarkers of PTE would enhance the temporal resolution of the ABCD Study(R)s PTE-related queries of tobacco use before and after learning of the pregnancy. Key Points- How does prenatal tobacco and/or alcohol exposure affect brain structure and longitudinal development in early adolescence? - Prenatal tobacco exposure was robustly associated with faster rates of cortical thinning in the frontal lobe; prenatal alcohol exposure had more minimal effects. - Prenatal substance exposure, especially prenatal tobacco exposure, not only affects cortical structure but how it develops long after those prenatal exposures occurred.

neuroscience↗

Longitudinal sex-at-birth and age analyses of cortical structure in the ABCD Study

While the brain continues to develop during adolescence, such development may depend on sex-at-birth. However, the elucidation of such differences may be hindered by analytical decisions (e.g., covariate selection to address body/brain-size differences) and the typical reporting of cross-sectional data. To further evaluate adolescent cortical development, we analyzed data from the Adolescent Brain Cognitive Development StudySM, whose cohort of 11,000+ youth participants with biannual neuroimaging data collection can facilitate understanding neuroanatomical change during a critical developmental window. Doubly considering individual differences in the context of group-level effects, we analyzed regional changes in cortical thickness, sulcal depth, surface area, and volume between two timepoints ([~]2 years apart) in 9-to 12-year-olds assigned male or female sex-at-birth. First, we conducted linear mixed-effects models to gauge how controlling for intracranial volume, whole-brain volume (WBV), or a summary metric (e.g., mean cortical thickness) influenced interpretations of age-dependent cortical change. Next, we evaluated the relative changes in thickness and surface area as a function of sex-at-birth and age. Here, we showed that WBV (thickness, sulcal depth, volume) and total cortical surface area were more optimal covariates; controlling for different covariates would have substantially altered our interpretations of overall and sex-at-birth-specific neuroanatomical development. Further, we provided evidence to suggest that aggregate change in how cortical thickness is changing relative to surface area is generally comparable across those assigned male or female sex-at-birth, with corresponding change happening at slightly older ages in those assigned male sex-at-birth. Overall, these results help elucidate neuroanatomical developmental trajectories in early adolescence. Significance StatementWhile most of our brains development happens early in life, much of it still happens in adolescence. Because many factors can alter those developmental trajectories, it is important to evaluate the shape/timing of those trajectories (i.e., what generally constitutes typical brain development). Here, we showed that our understanding of those trajectories can be affected by how we choose to analyze them. First, we showed that the way researchers address differences in brain/body size affects how we interpret regional variation in brain change over time. Further, we showed that it is important to consider how similar patterns of development may simply be happening at different ages in different groups. These results support a relatively novel way of analyzing adolescent brain development.

neuroscience↗

Relating neighborhood deprivation to childhood obesity in the ABCD Study(R): evidence for theories of neuroinflammation and neuronal stress

ObjectiveWe evaluated whether the relationships between area deprivation (ADI), body mass index (BMI) and brain structure (e.g., cortical thickness, subcortical volume) during pre-adolescence supported the neuroinflammation (NI) and/or neuronal stress (NS) theories of overeating. The NI theory proposes that ADI causes structural alteration in the brain due to the neuroinflammatory effects of overeating unhealthy foods. The NS theory proposes that ADI-related stress negatively impacts brain structure, which causes stress-related overeating and subsequent obesity. MethodsData were gathered from the Adolescent Brain Cognitive DevelopmentSM Study(R) (9-12-years-old; n=2872, 51.3% female). Linear mixed-effects models identified brain regions that were associated with both ADI and BMI; longitudinal mediation models assessed potential causal pathways. The NI model included ADI and BMI at 9/10-years-old and brain data at 11/12-years-old. The NS model included ADI and brain data at 9/10-years-old and BMI at 11/12-years-old. ResultsIn the NI model, BMI at 9/10-years-old positively mediated the relationship between AD and cortical thinning in the cuneus, lingual, and paracentral gyrus and larger volume of the Ventral DC at 11/12-years-old. In the NS model, cortical thinning in the lateral orbitofrontal cortex, lingual gyrus and larger volume of the Ventral DC at 9/10-years-old partially mediated the relationship between ADI and BMI at 11/12-years-old. ConclusionGreater area deprivation may indicate fewer access to resources that support healthy development, like nutritious food and non-stressful environments. Our findings provide evidence in support of the neuroinflammation and stress theories of overeating, specifically, with greater ADI influencing health outcomes of obesity via brain structure alterations.

neuroscience↗

Longitudinal assessment of brain structure and behavior in youth with rapid weight gain: Potential contributing causes and consequences

ObjectiveIndependent of weight status, rapid weight gain has been associated with underlying brain structure variation in regions associated with food intake and impulsivity among pre-adolescents. Yet, we lack clarity on how developmental maturation coincides with rapid weight gain and weight stability. MethodsWe identified brain predictors of two-year rapid weight gain and its longitudinal effects on brain structure and impulsivity in the Adolescent Brain Cognitive DevelopmentSM Study(R). Youth were categorized as Healthy Weight/Weight Stable (WSHW, n=225) or Weight Gainers (WG, n=221, >38lbs); 63% of the WG group were healthy weight at 9-to-10-years-old. ResultsA five-fold cross-validated logistic elastic-net regression revealed that rapid weight gain was associated with structural variation amongst 39 brain features at 9-to-10-years-old in regions involved with executive functioning, appetitive control, and reward sensitivity. Two years later, WG youth showed differences in change over time in several of these regions and performed worse on measures of impulsivity. ConclusionsThese findings suggest that brain structure in pre-adolescence may predispose some to rapid weight gain and that weight gain itself may alter maturational brain change in regions important for food intake and impulsivity. Behavioral interventions that target inhibitory control may improve trajectories of brain maturation and facilitate healthier behaviors.

neuroscience↗

Economic, social, and physiological resilience predict brain structure and cognitive performance in 9 - 10-year-old children

While children with economic disadvantage are at risk for poorer outcomes in cognitive and brain development, less understood is the contribution of other factors in the broader socioeconomic context that may more closely index the underlying mechanisms influencing risk and resilience. We examined brain structure and cognitive test performance in association with economic disadvantage and 22 measures in the broader socioeconomic context among n = 8,158 demographically diverse 9-10-year-old children from the ABCD Study. Total cortical surface area and total cognition scores increased as a function of income-to-needs, with the steepest differences most apparent among children below and near poverty relative to their wealthier peers. We found three latent factors encompassing distinct relationships among our proximal measures, including social, economic, and physiological well-being, each associated with brain structure and cognitive performance independently of economic advantage. Our findings will inform future studies of risk and resilience in developmental outcomes for children with economic disadvantage.

neuroscience↗

Image processing and analysis methods for the Adolescent Brain Cognitive Development Study

The Adolescent Brain Cognitive Development (ABCD) Study is an ongoing, nationwide study of the effects of environmental influences on behavioral and brain development in adolescents. The ABCD Study is a collaborative effort, including a Coordinating Center, 21 data acquisition sites across the United States, and a Data Analysis and Informatics Center (DAIC). The main objective of the study is to recruit and assess over eleven thousand 9-10-year-olds and follow them over the course of 10 years to characterize normative brain and cognitive development, the many factors that influence brain development, and the effects of those factors on mental health and other outcomes. The study employs state-of-the-art multimodal brain imaging, cognitive and clinical assessments, bioassays, and careful assessment of substance use, environment, psychopathological symptoms, and social functioning. The data will provide a resource of unprecedented scale and depth for studying typical and atypical development. Here, we describe the baseline neuroimaging processing and subject-level analysis methods used by the ABCD DAIC in the centralized processing and extraction of neuroanatomical and functional imaging phenotypes. Neuroimaging processing and analyses include modality-specific corrections for distortions and motion, brain segmentation and cortical surface reconstruction derived from structural magnetic resonance imaging (sMRI), analysis of brain microstructure using diffusion MRI (dMRI), task-related analysis of functional MRI (fMRI), and functional connectivity analysis of resting-state fMRI.\n\nHighlightsO_LIAn overview of the MRI processing pipeline for the ABCD Study\nC_LIO_LIA discussion on the challenges of large, multisite population studies\nC_LIO_LIA methodological reference for users of publicly shared data from the ABCD Study\nC_LI

neuroscience↗

Development of subcortical volumes across adolescence in males and females: A multisample study of longitudinal changes

The developmental patterns of subcortical brain volumes in males and females observed in previous studies have been inconsistent. To help resolve these discrepancies, we examined developmental trajectories using three independent longitudinal samples of participants in the age-span of 8-22 years (total 216 participants and 467 scans). These datasets, including Pittsburgh (PIT; University of Pittsburgh, USA), NeuroCognitive Development (NCD; University of Oslo, Norway), and Orygen Adolescent Development Study (OADS; The University of Melbourne, Australia), span three countries and were analyzed together and in parallel using mixed-effects modeling with both generalized additive models and general linear models. For all regions and across all samples, males were found to have significantly larger volumes as compared to females, and significant sex differences were seen in age trajectories over time. However, direct comparison of sample trajectories and sex differences identified within samples were not consistent. The trajectories for the amygdala, putamen, and nucleus accumbens were most consistent between the three samples. Our results suggest that even after using similar preprocessing and analytic techniques, additional factors, such as image acquisition or sample composition may contribute to some of the discrepancies in sex specific patterns in subcortical brain changes across adolescence, and highlight region-specific variations in congruency of developmental trajectories.

neuroscience↗