30263
Neural Architecture of Default Mode Network during Social Interaction in Autism Spectrum Disorder and Schizophrenia: Categorical Vs. Dimensional Approaches
Although autism spectrum disorder (ASD) and schizophrenia (SZ) are considered separate clinical entities, deficits in core social function are characteristic of both. Social function depends on complex interwoven processes that lie on a continuum, encompassing clinical and non-clinical populations. However, the dimensionality of social-cognitive processes across ASD and SZ samples, and delineation of common or disparate neural mechanisms, have yet to be determined.
Objectives:
We aimed to (1) characterize latent social processing constructs based on multiple social cognitive measures and assess their dimensionality, differences, and overlaps between healthy young adults and clinical samples of ASD and SZ participants; (2) delineate the functional connectivity (FC) within the default mode network (DMN), a neural network shown to be involved in social processes, while individuals engaged in a social competitive game during functional MRI (fMRI) scanning; and (3) determine whether FC measures better aligned with categorical diagnosis of ASD or SZ or with dimensional social constructs.
Methods:
Forty-two adults with high-functioning ASD, 60 with SZ and 73 healthy participants (mean age=26.1±7.4 years) completed a battery of social-cognitive measures, and a competitive Domino fMRI task. Exploratory factor analysis (EFA) was used to identify latent social constructs from social-cognitive scores and group differences were assessed with ANCOVA. FC was computed using high-order independent component analysis (ICA; 75 component estimated). Ten DMN components were selected and mentalizing-specific beta weights, reflecting the degree to which brain regions included in a component are modulated by the mentalizing condition, were calculated during a task-interval when participants attempted to predict the other player’s next move. ANCOVAs were used to estimate the effect of diagnosis and social factors on components’ beta values. All analyses were controlled for age, gender and estimated IQ.
Results:
EFA revealed 5 social factors interpreted as mentalizing and empathy (F1), social distress (F2) social-emotional perception (F3), fantasizing/daydreaming (F4) and self-emotion processing (F5). Factors 1, 2, 3 and 5 differed by diagnostic group (F>6.6, p<.002), with ASD and SZ distinguished from healthy participants but not from each other. Inspection of the factor loadings demonstrated clear overlap and continuous distribution between all 3 groups. Similarly, ASD and SZ showed decreased DMN FC during mentalizing relative to healthy particiapnts in posterior cingulate cortex and bilateral temporoparietal junctions (F>6.38, p<.01). An interaction between diagnosis and F2 (social distress) was found in subgenual anterior cingulate cortex (sgACC; F=5.9, p=.005), such that SZ showed negative association between F2 and sgACC connectivity, significantly differing from ASD (p=.05) and healthy individuals (p=.001).
Conclusions:
The current study delineates five dimensional social constructs across SZ, ASD, and non-clinical individuals. While four showed significant differences between the clinical and non-clinical groups, ASD and SZ overlapped in ability. Similar patterns were observed in neural connectivity within posterior and lateral regions of the DMN. However, when taking into account social factors, a significant difference between ASD and SZ was identified in the ACC in relation to social distress, suggesting that categorical and dimensional approaches are complementary and should be taken into account during individual assessment and treatment.