COGNITION AND FUNCTIONAL OUTCOMES IN SCHIZOPHRENIA Highlights • Meta-analysis of 166 studies (12,868 individuals) examining relationships between neurocognition and social cognition and functional outcomes. • Domains of neurocognition and social cognition demonstrate small to medium relationships with functional outcomes. • Neurocognition and social cognition did not demonstrate significantly different relationships with functional outcomes, however, social cognition domains explained more unique variance. • Social cognition is a partial mediator between neurocognition and functional outcomes.

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Roughly twenty years of functional magnetic resonance imaging (fMRI) studies have investigated the neural correlates underlying engagement in social cognition (e.g., empathy, emotion perception) about targets spanning various social categories (e.g., race, gender). Yet findings from individual studies remain mixed. In the present quantitative functional neuroimaging meta-analysis, we summarized across 50 fMRI studies of social cognition to identify consistent differences in neural activation as a function of whether the target of social cognition was an ingroup or outgroup member. We investigated if such differences varied according to social category (i.e., race) and social cognitive process (i.e., empathy, emotion perception). We found that social cognition about ingroup members was more reliably related to activity in brain regions associated with mentalizing (e.g., dmPFC), whereas social cognition about outgroup members was more reliably related to activity in regions associated with exogenous attention and salience (e.g., anterior insula). These findings replicated for studies specifically focused on the social category of race, and we further found intergroup differences in neural activation during empathy and emotion perception tasks. These results help shed light on the neural mechanisms underlying social cognition across group lines.

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Racial disparities in health are a major public health problem in the United States, especially when comparing chronic disease morbidity and mortality for Black versus White Americans. These health disparities are primarily due to insidious anti-Black racism that permeates American history, current culture and institutions, and interpersonal interactions. But how does racism get under the skull and the skin to influence brain and bodily processes that impact the health of Black Americans? In the present article, we present a model describing the possible neural and inflammatory mechanisms linking racism and health. We hypothesize that racism influences neural activity and connectivity in the salience and default mode networks of the brain and disrupts interactions between these networks and the executive control network. This pattern of neural functioning in turn leads to greater sympathetic nervous system signaling, hypothalamic-pituitary-adrenal axis activation, and increased expression of genes involved in inflammation, ultimately leading to higher levels of proinflammatory cytokines in the body and brain. Over time, these neural and physiological responses can lead to chronic physical and mental health conditions, disrupt wellbeing, and cause premature mortality. Given that research in this area is underdeveloped to date, we emphasize opportunities for future research that are needed to build a comprehensive mechanistic understanding of the brain-body pathways linking anti-Black racism and health.