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Cortical Correlates of Subclinical Antisocial Behaviors Open Access

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Antisocial disorders, such as psychopathy, are characterized by impairments in social-emotional functioning. Individuals presenting with these disorders are known to have distinct structural, particularly gray matter, brain abnormalities. However, comorbidities (e.g., ADHD, drug use and abuse, etc.) in these clinical disorders can often cloud our understanding of the specific contributions of these behaviors to brain-based atypicalities. Subclinical behaviors associated with antisocial disorders are also present in the general, typically developing population and allow for an unobscured approach to linking brain with these behaviors. The present study investigates links between antisocial traits and cortical structure within a large sample of young adults screened for the presence of psychiatric and neurological impairments. In the current study we correlate variation in a metric of gray matter structure, cortical thickness, across the entire cortex with scores on a measure of antisocial traits, the Self-Report Psychopathy-Fourth Edition-Short Form (SRP4-SF), which is composed of four subtests: Interpersonal, Affective, Lifestyle, and Antisocial. 694 typically developing young adults (280 male: 414 female) completed the questionnaire and provided MRI scans. The CIVET brain-imaging pipeline (v2.0) and SurfStat were used to derive vertex-level cortical thickness values (>80,000 vertices) and complete analyses. Broadly speaking, the results showed thinner cortex in prefrontal areas (e.g., bilateral superior and medial frontal and anterior cingulate cortices) with increasing antisocial traits. These findings complement the current literature on groups with frank antisocial behavior, which are characterized by thinner cortices in these same areas (Yang et al., 2012; Yang et al., 2015). Furthermore, they provide support to the notion that these results generalize to subclinical populations. Since such social-emotional behaviors are continuous and present in the general population, these results may aid the detection and classification of neural endophenotypes that will inform not only our understanding of antisocial disorders, but also the etiology (including genetic underpinnings) of individual differences in social-emotional functioning.

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