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.

Growing evidence indicates that risk for bipolar disorder is characterized by elevated activation in a fronto-striatal reward neural circuit involving the ventral striatum and orbitofrontal cortex, among other regions. It is proposed that individuals with abnormally elevated reward-related neural activation are at risk for experiencing an excessive increase in approach-related motivation during life events involving rewards or goal striving and attainment. In the extreme, this increase in motivation is reflected in hypomanic/manic symptoms. By contrast, unipolar depression (without a history of hypomania/mania) is characterized by decreased reward responsivity and decreased reward-related neural activation. Collectively, this suggests that risk for bipolar disorder and unipolar depression are characterized by distinct and opposite profiles of reward processing and reward-related neural activation. The objective of the present paper is threefold. First, we review the literature on reward processing and reward-related neural activation in bipolar disorder, and in particular risk for hypomania/mania. Second, we propose that reward-related neural activation reflects a biological marker of differential risk for bipolar disorder versus unipolar depression that may help facilitate psychiatric assessment and differential diagnosis. We also discuss, however, the challenges to using neuroscience techniques and biological markers in a clinical setting for assessment and diagnostic purposes. Lastly, we address the pharmacological and psychosocial treatment implications of research on reward-related neural activation in bipolar disorder.

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Sleep deprivation and disorders are linked to reduced DMn connectivity. Less is known about how naturalistic sleep patterns -specifically sleep irregularity -relate to the DMN, particularly among adolescents and young adults. Additionally, no studies have utilized graph theory analysis to clarify whether sleep-related decreases in connectivity reflect global or local DMN changes. Twenty-five healthy adolescents and young adults (age range = 12-22; mean = 18.08; SD = 2.64, 56% female) completed 7 days of actigraphy and resting-state fMRI. Sleep regularity was captured by the Sleep Regularity Index (SRI) and the relationship between the SRI and DMN was examined using graph theory analysis. Analogous analyses explored relationships between the SRi and additional resting-state networks. Greater sleep regularity related to decreased path length (increased network connectivity) in DMn regions, particularly the right and left lateral parietal lobule, and the Language network, including the left inferior frontal gyrus and the left posterior superior frontal gyrus. findings were robust to covariates including sex and age. Sleep and DMn function may be tightly linked during adolescence and young adulthood, and reduced DMN connectivity may reflect local changes within the network. future studies should assess how this relationship impacts cognitive development and neuropsychiatric outcomes in this age group. open Scientific RepoRtS | (2020) 10:509 | https://doi.complaints are often observed among adolescents with neuropsychiatric conditions, such as ADHD, depression, and emerging psychosis 17,18,[57][58][59][60] , future studies should examine how the interplay between sleep regularity and DMN connectivity and network structure impacts the presentation of these disorders during this developmental period.Indeed, a recent study has shown that poor sleep quality is related to increased impulsivity among adolescents with low, but not high, connectivity between the DMN and prefrontal cortex, suggesting DMN connectivity may contribute to links between sleep and behavioral outcomes in this age group 61 . Additionally, another recent investigation has suggested that greater sleep irregularity, as measured by the SRI, may mediate the relationship between delayed sleep onset time and daytime functioning in work/school, social, and family domains 62 . Finally, exploratory analysis in the current study indicated a relationship between sleep regularity and network structure efficiency within the Language Network, particularly in areas of the left inferior frontal gyrus and the left posterior superior frontal gyrus. Relative to the DMN, very little is known about how sleep may relate to connectivity within this network. However, it is notable that from a behavioral perspective, sleep irregularity in general has been linked to poorer verbal cognition in youth 21 and the SRI specifically is associated with poorer communication among youth with Autism 63 . Future investigations using larger samples of adolescents and young adults should rep...

The Reward Hypersensitivity Model of bipolar disorder argues that hypersensitivity to reward-relevant cues characterizes risk for hypo/mania. This hypersensitivity leads to increased goal-directed motivation during reward-relevant life events that, in the extreme, is reflected in hypo/manic symptoms. In line with this perspective, individuals with bipolar disorder display elevated activation in a cortico-striatal reward circuit including the nucleus accumbens (NAcc) and medial orbitofrontal cortex (mOFC). To date, however, research on reward-related neural circuitry underlying bipolar symptoms focuses on syndromal bipolar disorder (bipolar I, bipolar II), and typically examines neural regions in isolation of each other. Accordingly, this study examines the relationship between subsyndromal hypo/mania proneness and structural connectivity between the NAcc and both the mOFC and amygdala in a medication-free sample. Fifty-four community participants completed diffusion-weighted imaging and a self-report measure of bipolar risk (hypo/mania proneness). As predicted, elevated structural connectivity between the NAcc and both the mOFC and amygdala were associated with elevated hypo/mania proneness. This relationship was specific to NAcc-centered reward connectivity, as there was no relationship between hypo/mania proneness and either whole-brain or cortico-amygdala connectivity. Results suggest that reward-relevant tractography from cortical (mOFC) and subcortical (amygdala) regions amplify NAcc-centered reward processing in bipolar risk.