Examining the association between exposome score for schizophrenia and functioning in schizophrenia, siblings, and healthy controls: Results from the EUGEI study
Date
2021Author
GÜMÜŞ-AKAY, GÜVEM
Andric-Petrovic, Sanja
Mirjanic, Tijana
Bernardo, Miguel
Mezquida, Gisela
Amoretti, Silvia
Bobes, Julio
Saiz, Pilar A.
Garcia-Portilla, Maria Paz
Sanjuan, Julio
Aguilar, Eduardo J.
Santos, Jose Luis
Jimenez-Lopez, Estela
Arrojo, Manuel
Carracedo, Angel
Lopez, Gonzalo
Gonzalez-Penas, Javier
Parellada, Mara
Maric, Nadja P.
Atbasoglu, Cem
Ucok, Alp
ALPTEKİN, KÖKSAL
Saka, Meram Can
Arango, Celso
O'Donovan, Micheal C.
Rutten, Bart P. F.
Guloksuz, Sinan
Erzin, Gamze
Pries, Lotta-Katrin
van Os, Jim
Fusar-Poli, Laura
Delespaul, Philippe
Kenis, Gunter
Luykx, Jurjen J.
Lin, Bochao D.
Richards, Alexander L.
Akdede, Berna
Binbay, Tolga
ALTINYAZAR, VESİLE
Yalincetin, Berna
CİHAN, BURÇİN
Soygur, Haldun
ULAŞ, HALİS
Cankurtaran, Eylem Sahin
Kaymak, Semra Ulusoy
Mihaljevic, Marina M.
Metadata
Show full item recordAbstract
Background A cumulative environmental exposure score for schizophrenia (exposome score for schizophrenia [ES-SCZ]) may provide potential utility for risk stratification and outcome prediction. Here, we investigated whether ES-SCZ was associated with functioning in patients with schizophrenia spectrum disorder, unaffected siblings, and healthy controls. Methods This cross-sectional sample consisted of 1,261 patients, 1,282 unaffected siblings, and 1,525 healthy controls. The Global Assessment of Functioning (GAF) scale was used to assess functioning. ES-SCZ was calculated based on our previously validated method. The association between ES-SCZ and the GAF dimensions (symptom and disability) was analyzed by applying regression models in each group (patients, siblings, and controls). Additional models included polygenic risk score for schizophrenia (PRS-SCZ) as a covariate. Results ES-SCZ was associated with the GAF dimensions in patients (symptom: B = -1.53, p-value = 0.001; disability: B = -1.44, p-value = 0.001), siblings (symptom: B = -3.07, p-value B = -2.52, p-value < 0.001), and healthy controls (symptom: B = -1.50, p-value B = -1.31, p-value < 0.001). The results remained the same after adjusting for PRS-SCZ. The degree of associations of ES-SCZ with both symptom and disability dimensions were higher in unaffected siblings than in patients and controls. By analyzing an independent dataset (the Genetic Risk and Outcome of Psychosis study), we replicated the results observed in the patient group. Conclusions Our findings suggest that ES-SCZ shows promise for enhancing risk prediction and stratification in research practice. From a clinical perspective, ES-SCZ may aid in efforts of clinical characterization, operationalizing transdiagnostic clinical staging models, and personalizing clinical management.
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