Evidence of discontinuity between psychosis-risk and non-clinical samples in the neuroanatomical correlates of social function
: Haas Shalaila S, Doucet Gaelle E, Antoniades Mathilde, Modabbernia Amirhossein, Corcoran Cheryl M, Kahn René S, Kambeitz Joseph, Kambeitz-Ilankovic Lana, Borgwardt Stefan, Brambilla Paolo, Upthegrove Rachel, Wood Stephen J, Salokangas Raimo K R, Hietala Jarmo, Meisenzahl Eva, Koutsouleris Nikolaos, Frangou Sophia
Publisher: Elsevier Inc.
: 2022
: Schizophrenia research: cognition
: Schizophrenia Research: Cognition
: 29
: 2215-0013
DOI: https://doi.org/10.1016/j.scog.2022.100252
: https://doi.org/10.1016/j.scog.2022.100252
: https://research.utu.fi/converis/portal/detail/Publication/175207250
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.
