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Social dysfunction is common across psychiatric disorders, including depressive and anxiety disorders. Both disorders have been associated with negative biases in socioaffective neural processing, which may impact responses to social stimuli. This study aims to determine whether social dysfunction across these psychiatric disorders is indeed coupled to altered neural processing of negative and positive valenced emotional stimuli and whether a common neurobiological correlate can be identified. An implicit emotional faces functional magnetic resonance imaging task was used to measure brain activation in response to emotional stimuli in participants with depression (N = 46), anxiety (N = 45), comorbid depressive and anxiety disorders (N = 57), and healthy controls (N = 52). Social dysfunction was indexed using five items of the World Health Organisation Disability Assessment Schedule‐2.0 (i.e., perceived social disability) and with the De Jong‐Gierveld Loneliness scale (LON; i.e., perceived loneliness). Higher perceived social disability scores were associated with greater brain activation in the left angular gyrus in response to sad emotional faces across all participants but did not correlate with responses to overall negative (sad, angry, and fearful) or positive (happy) emotional faces. No interaction effect of diagnosis was observed for the finding. Perceived loneliness scores did not correlate with brain activation to emotional faces. Taken together, perceived social disability across persons with and without depressive and/or anxiety disorders converges specifically on sad emotional processing of the left angular gyrus, suggesting a potential common neurobiological correlate for social dysfunction. [ABSTRACT FROM AUTHOR]

Background. Long-term comorbidities such as cognitive impairment remain prevalent in otherwise effectively treated people living with human immunodeficiency virus (HIV). We investigate the relationship between cognitive impairment and brain structure in successfully treated patients using multimodal neuroimaging from the Comorbidity in Relation to AIDS (COBRA) cohort. Methods. Cognitive function, brain tissue volumes, and white matter microstructure were assessed in 134 HIV-infected patients and 79 controls. All patients had suppressed plasma HIV RNA at cohort entry. In addition to comprehensive voxelwise analyses of volumetric and diffusion tensor imaging, we used an unsupervised machine learning approach to combine cognitive, diffusion, and volumetric data, taking advantage of the complementary information they provide. Results. Compared to the highly comparable control group, cognitive function was impaired in 4 of the 6 cognitive domains tested (median global T-scores: 50.8 vs 54.2; P < .001). Patients had lower gray but not white matter volumes, observed principally in regions where structure generally did not correlate with cognitive function. Widespread abnormalities in white matter microstructure were also seen, including reduced fractional anisotropy with increased mean and radial diffusivity. In contrast to the gray matter, these diffusion abnormalities correlated with cognitive function. Multivariate neuroimaging analysis identified a neuroimaging phenotype associated with poorer cognitive function, HIV infection, and systemic immune activation. Conclusions. Cognitive impairment, lower gray matter volume, and white matter microstructural abnormalities were evident in HIV-infected individuals despite fully suppressive antiretroviral therapy. White matter abnormalities appear to be a particularly important determinant of cognitive dysfunction seen in well-treated HIV-infected individuals. [ABSTRACT FROM AUTHOR]