TY - JOUR
T1 - Evidence of discontinuity between psychosis-risk and non-clinical samples in the neuroanatomical correlates of social function
AU - Haas, Shalaila S.
AU - Doucet, Gaelle E.
AU - Antoniades, Mathilde
AU - Modabbernia, Amirhossein
AU - Corcoran, Cheryl M.
AU - Kahn, René S.
AU - Kambeitz, Joseph
AU - Kambeitz-Ilankovic, Lana
AU - Borgwardt, Stefan
AU - Brambilla, Paolo
AU - Upthegrove, Rachel
AU - Wood, Stephen J.
AU - Salokangas, Raimo K.R.
AU - Hietala, Jarmo
AU - Meisenzahl, Eva
AU - Koutsouleris, Nikolaos
AU - Frangou, Sophia
N1 - Publisher Copyright:
© 2022 The Authors
PY - 2022/9
Y1 - 2022/9
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85127527944&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/a7680fc0-9204-3f26-bd8d-4e719f7fd34a/
U2 - 10.1016/j.scog.2022.100252
DO - 10.1016/j.scog.2022.100252
M3 - Journal articles
C2 - 35391789
AN - SCOPUS:85127527944
SN - 2215-0013
VL - 29
SP - 100252
JO - Schizophrenia Research: Cognition
JF - Schizophrenia Research: Cognition
M1 - 100252
ER -