T255. Neurobiological Substrates of Social Cognitive Clusters in Schizophrenia Spectrum Disorders: A Multimodal Approach


Verim B., Dokuyan Y., Demir M., Demirlek C., Kucukakdag A., Cesim E., ...Daha Fazla

2026 ANNUAL CONGRESS of the Schizophrenia International Research Society, Florence, İtalya, 25 - 29 Mart 2026, ss.558-559, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Florence
  • Basıldığı Ülke: İtalya
  • Sayfa Sayıları: ss.558-559
  • Dokuz Eylül Üniversitesi Adresli: Evet

Özet

Background: Social cognitive deficits are a hallmark of schizophrenia spectrum disorders (SSD). Individuals with SSD exhibit marked impairments across multiple domains of social cognition, including theory of mind, emotion recognition, social perception, and social knowledge. These social cognitive difficulties have been associated with clinical outcomes and functioning, as well as alterations in brain structure and functional organization. However, there is substantial heterogeneity in social cognitive impairment in SSD, and its underlying neural mechanisms are not yet well characterized. The present study aimed to examine the neurobiological characteristics of social cognitive clusters in this patient group.

Methods: The sample consisted of 82 individuals with SSD and 40 healthy controls. Participants underwent comprehensive clinical evaluations and a cognitive assessment battery, followed by T1-weighted, diffusion-weighted, and resting-state functional MRI scans. Clinical evaluations included the Hamilton Depression Scale, the Scale for the Assessment of Positive Symptoms, the Brief Negative Symptom Scale, the Premorbid Adjustment Scale, and the Personal and Social Performance Scale. The cognitive battery included both neurocognitive and social cognitive measures. The Screen for Cognitive Impairment in Psychiatry (SCIP) was used to assess neurocognitive performance. The social cognitive battery included the Penn Emotion Recognition Test (Penn-40), Reading the Mind in the Eyes Test (RMET), the Modified Hinting Task, the Profile of Nonverbal Sensitivity (PONS), the Social Norms Questionnaire (SNQ), and the Face Trustworthiness Task. Social cognitive clusters were identified using latent profile analysis based on theory of mind (RMET, the Modified Hinting Task), emotion recognition (Penn-40), social perception (PONS, Face Trustworthiness Task), and social knowledge (SNQ) domains. Preprocessing and analysis of the structural, diffusion, and functional MRI data were conducted using FreeSurfer, FSL, and fMRIPrep, respectively.

Results: Latent profile analysis (LPA) identified two clusters in the patient group: mild (N=44) and severe (N=38) social cognitive impairment. Although the groups showed comparable clinical features, the severely impaired subgroup demonstrated markedly poorer performance on both neurocognitive and social cognitive tasks than the mildly impaired subgroup and healthy controls. Both groups showed structural abnormalities relative to controls, with the mild group demonstrating reductions in frontal and temporal regions and the severe group showing more widespread cortical and subcortical abnormalities. The severe subgroup also exhibited greater abnormalities than the mild group, particularly in frontal and

occipital regions. Both subgroups displayed altered local gyrification in frontal and parietal cortices. Compared with healthy controls, the severely impaired subgroup demonstrated widespread decrease in resting-state functional connectivity across multiple large-scale networks. This group showed significantly decreased within-network connectivity in the somatomotor, visual, default mode, and frontoparietal networks. Furthermore, they exhibited decreased between-network connectivity, particularly between the default mode and salience networks, as well as between the default mode and subcortical networks.

Discussion: The most prominent finding was the presence of more widespread and consistent structural and connectivity alterations in the severely impaired group. These findings indicate that variability in social cognitive ability among individuals with SSD aligns with distinct morphological and connectivity profiles. Identifying these neurobiological patterns provides evidence for more biologically valid clinical syndromes and may support efforts to establish more precise neural markers and develop individualized treatment strategies in schizophrenia.