A unified general cognitive factor explains impairment across schizophrenia, bipolar disorder, OCD and substance use disorder.
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Jayasankar Pavithra, Balachander Srinivas, Nayok Swarna Buddha, Singh Arushi, Dayalamurthy Pavithra, Joseph Mino Susan, Das Aswathy, Bhattacharya Mahashweta, Shaktan Alka, Hiremath Chandrakanta S, Solanki Aishwarya L, Jayaraj Gopika, Sreenivasalu Mallappagiri, N Shruthi, R Alagarsami A, Syed Farooq Ali, Vinod Pratibha, Teotia Vasundhra, Kurian Aina, V Nikhilan J, K Rajkumar, Arampady Chidatma, Manideepika Tallapally, Shareen Shama, T Arsharani P, V Manjula, Ithal Dhruva, Mahadevan Jayant, Nadella Ravi Kumar, Sreeraj Vanteemar S, Venkatasubramanian Ganesan, John John P, Benegal Vivek, Reddy Yc Janardhan, Varghese Mathew, Jain Sanjeev, Mehta Urvakhsh Meherwan, Holla Bharath, Viswanath Biju, ADBS-CBM Consortium, Sivakumar Palanimuthu T, Kandasamy Arun, Mehta Bhupesh, Kandavel Thennarasu, Binukumar Bhaskarapillai, Saini Jitender, Kesavan Muralidharan, Arumugham Shyam Sundar, Kg Vijay Kumar, Shukla Lekhansh, Suhas Satish, Harbishettar Vijay Kumar, Reddy Preethi, Ganesh Suhas, Sud Reeteka, Purushottam Meera, Ks Meena, Latha K, U Gautam Arunachal, Cherian Anish V, Kashyap Himani, Snm Ashitha, Paul Pradip, Ms Bhagyalakshmi, Thirthalli Jagadisha, Chandra Prabha S, Murthy Pratima, Bhalla Upinder S, Raghu Padinjat
Аннотация
METHODS: A total of 797 individuals [544 affected and 253 healthy controls (HC)] completed a standardized cognitive battery. Bifactor confirmatory factor analysis was used to derive general cognitive factor (gFc) and domain-specific impairments (cognitive flexibility, working memory, new learning and social cognition). Model fit supported the bifactor structure. Linear mixed-effect models, with family as random effect, and demographic variables as fixed effect evaluated transdiagnostic and diagnosis specific impairments.
RESULTS: The gFc was significantly reduced across all diagnoses groups relative to HC, [B(SE): BD -0.49 (0.07), OCD -0.21 (0.07), SUD -0.43(0.08), SZ -0.76 (0.08), all p < 0.001]; verbal learning showed additional diagnosis-specific deficits, most pronounced in SZ [B (SE):0.59 (0.09)] and BD[B(SE):0.48 (0.09)], both p < 0.001.
CONCLUSION: A single gFc accounts for substantial cognitive dysfunction across major psychiatric disorders, while verbal-learning impairment appears diagnosis-specific. These findings support a dimensional architecture of cognition in psychiatry and identify gFc as a promising transdiagnostic target for clinical and mechanistic research.