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Evidence of discontinuity between psychosis-risk and non-clinical samples in the neuroanatomical correlates of social function

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Meisenzahl,  Eva
Max Planck Institute of Psychiatry, Max Planck Society;

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Koutsouleris,  Nikolaos
Max Planck Fellow Group Precision Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Haas, S. S., Doucet, G. E., Antoniades, M., Modabbernia, A., Corcoran, C. M., Kahn, R. S., et al. (2022). Evidence of discontinuity between psychosis-risk and non-clinical samples in the neuroanatomical correlates of social function. SCHIZOPHRENIA RESEARCH-COGNITION, 29: 100252. doi:10.1016/j.scog.2022.100252.


Cite as: https://hdl.handle.net/21.11116/0000-000A-D470-8
Abstract
Objective: Social dysfunction is a major feature of clinical-high-risk states for psychosis (CHR-P). Prior research has identified a neuroanatomical pattern associated with impaired social function outcome in CHR-P. The aim of the current study was to test whether social dysfunction in CHR-P is neurobiologically distinct or in a continuum with the lower end of the normal distribution of individual differences in social functioning. Methods: We used a machine learning classifier to test for the presence of a previously validated brain structural pattern associated with impaired social outcome in CHR-P (CHR-outcome-neurosignature) in the neuroimaging profiles of individuals from two non-clinical samples (total n = 1763) and examined its association with social function, psychopathology and cognition. Results: Although the CHR-outcome-neurosignature could be detected in a subset of the non-clinical samples, it was not associated was adverse social outcomes or higher psychopathology levels. However, participants whose neuroanatomical profiles were highly aligned with the CHR-outcome-neurosignature manifested subtle disadvantage in fluid (PFDR = 0.004) and crystallized intelligence (PFDR = 0.01), cognitive flexibility (PFDR = 0.02), inhibitory control (PFDR = 0.01), working memory (PFDR = 0.0005), and processing speed (PFDR = 0.04). Conclusions: We provide evidence of divergence in brain structural underpinnings of social dysfunction derived from a psychosis-risk enriched population when applied to non-clinical samples. This approach appears promising in identifying brain mechanisms bound to psychosis through comparisons of patient populations to nonclinical samples with the same neuroanatomical profiles.