Neurocognition and social cognition as risk markers in adolescents: a comparative study of asymptomatic siblings of Early-Onset Schizophrenia and bipolar disorder
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s00406-026-02394-9
- Dergi Adı: EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE, Psycinfo, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest), Psychology & Behavioral Sciences Collection (EBSCO)
- Bursa Uludağ Üniversitesi Adresli: Evet
Özet
Early-Onset Schizophrenia (EOS) and Early-Onset Bipolar Disorder (EOBD) share overlapping clinical and genetic features. This study aims to compare the neuro-social cognitive performance of healthy siblings of adolescents with EOS (EOS-Sib) and EOBD (EOBD-Sib) to identify candidate neurocognitive markers of familial liability and evaluate the impact of environmental stressors, such as childhood trauma, on neurocognitive and social cognitive performance. The study included 164 participants: 36 EOS-Sib, 40 EOBD-Sib, and 88 healthy controls (HC) aged 11-23. All subjects underwent a rigorous screening process using the semi structured interview (K-SADS-PL) to exclude any psychopathology. Neuro-social cognitive performance was assessed using the University of Pennsylvania Computerized Neurocognitive Battery. Also, Childhood Trauma Questionnaire and Children's Depression Rating Scale are used for the clinical evaluation. A composite 'G-score' was derived to represent global neurocognitive performance. Although both sibling groups differed from healthy controls on selected neurocognitive measures, no significant differences were detected between the EOS-Sib and EOBD-Sib groups, indicating substantial overlap in neurocognitive performance across the two familial-risk groups. This null finding suggests shared transdiagnostic neurocognitive vulnerability rather than disorder-specific cognitive differentiation at the familial-risk level. After controlling for age, maternal education, paternal education, depressive symptom severity, and childhood trauma, both EOS-Sib and EOBD-Sib groups exhibited significant deficits in global neurocognitive performance compared to healthy controls (p < .001). For emotion recognition (ER), a significant impairment was observed only in the EOS-Sib group (p = .003). Childhood trauma was independently associated with poorer ER performance (p = .007), but was not significantly associated with general neurocognitive performance (p = .746). The Neurocognitive G-score demonstrated good group-level discriminative ability between adolescents with familial liability and healthy controls (AUC = 0.805). In conclusion, unaffected siblings of adolescents with EOS and EOBD exhibited overlapping neurocognitive impairments, particularly in executive functioning and working memory, supporting these domains as candidate neurocognitive markers associated with familial liability. The Neurocognitive G-score demonstrated good group-level discriminative ability between adolescents with known familial liability and healthy controls; however, it should be regarded as an exploratory neurocognitive risk indicator rather than a definitive screening tool, and longitudinal studies are needed to determine its prognostic value for future psychopathology. Furthermore, childhood trauma was independently associated with poorer ER performance after adjustment for relevant covariates, highlighting the potential contribution of environmental adversity to social cognitive functioning in at-risk adolescents.