AbstractIntroduction: Schizophrenia symptomatology exists on a continuum ranging from subclinical psychotic-like experiences in the general population (schizotypy) to full-blown clinical symptoms. High schizotypy individuals are at an increased risk for developing clinical diagnoses, yet previous work has not investigated key neural abnormalities of schizophrenia in these samples.
Methods: To ensure findings are informative for clinical risk, we only recruited individuals scoring at the extreme low/high end of the Schizotypy Personality Questionnaire. 27 high schizotypy (HS) and 26 low schizotypy (LS) individuals to take part in two functional magnetic resonance imaging (fMRI) tasks assessing social learning. Participants also underwent a resting state fMRI and a magnetic resonance spectroscopy scan.
Results: HS subjects, compared to LS, present with abnormal learning of social information. HS overestimate the volatility of social cues and are slower to learn about global changes in social context. Furthermore, HS subjects show reduced neural activity in the dopaminergic midbrain and increased frontal cortex activity in response to prediction errors during social learning. HS subjects also present with a reduced resting-state functional connectivity between hippocampus and striatum/thalamus and with reduced GABA and Glu metabolite levels in the prefrontal cortex.
Discussion: HS subjects, representing the earliest risk for clinical transition to schizophrenia, already present with key neural abnormalities implicated in progression, mainly abnormal hippocampal functioning and abnormal GABA/Glu levels. These results encourage investigations of HS to facilitate a comprehensive view of risk/protective factors for clinical transition. The results also show that HS subjects already present with abnormal hierarchical learning as seen in clinical samples. HS subjects neutrally underweight prediction errors indicating an improper processing of these learning cues. They also present with compensatory activity in frontal cortex enabling behavioural performance similar to LS. The abnormal learning from social cues could explain not only the social functioning deficits key to schizophrenia, but also other cognitive biases observed in these populations.
|Date of Award||6 May 2021|
|Sponsors||Roehampton VC Scholarship|
|Supervisor||Paul Allen (Director of Studies) & Andreea Diaconescu (Co-Supervisor)|
- psychosis risks
- social cognition
- computational analysis