Schizophrenia Research: Cognition (Sep 2022)

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

  • Shalaila S. Haas,
  • Gaelle E. Doucet,
  • Mathilde Antoniades,
  • Amirhossein Modabbernia,
  • Cheryl M. Corcoran,
  • René S. Kahn,
  • Joseph Kambeitz,
  • Lana Kambeitz-Ilankovic,
  • Stefan Borgwardt,
  • Paolo Brambilla,
  • Rachel Upthegrove,
  • Stephen J. Wood,
  • Raimo K.R. Salokangas,
  • Jarmo Hietala,
  • Eva Meisenzahl,
  • Nikolaos Koutsouleris,
  • Sophia Frangou

Journal volume & issue
Vol. 29
p. 100252

Abstract

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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 non-clinical samples with the same neuroanatomical profiles.

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