Yilmaz Kafali, H.Dasgin, HacerSahin Cevik, DidenurSozan, S. S.Oguz, Kader K.Mutlu, M.Ozkaya Parlakay, A.Toulopoulou, Timothea2024-03-112024-03-112023-120925-4927https://hdl.handle.net/11693/114465We first aimed to investigate resting-state functional connectivity (rs-FC) differences between adolescents exposed to SARS-CoV-2 and healthy controls. Secondly, the moderator effect of PLEs on group differences in rs-FC was examined. Thirdly, brain correlates of inflammation response during acute SARS-CoV-2 infection were investigated. Eighty-two participants aged between 14 and 24 years (SARS-CoV-2 (n = 35), controls (n = 47)) were examined using rs-fMRI. Seed-based rs-FC analysis was performed. The positive subscale of Community Assessment of Psychotic Experiences-42 (CAPE-Pos) was used to measure PLEs. The SARS-CoV-2 group had a lesser rs-FC within sensorimotor network (SMN), central executive network (CEN) and language network (LN), but an increased rs-FC within visual network (VN) compared to controls. No significant differences were detected between the groups regarding CAPE-Pos-score. However, including CAPE-Pos as a covariate, we found increased rs-FC within CEN and SN in SARS-CoV-2 compared to controls. Among the SARS-CoV-2 group, neutrophil/lymphocyte and thrombocyte*neutrophil/lymphocyte ratio was correlated with decreased/increased FC within DMN and SN, and increased FC within CEN. Our results showed rs-FC alterations within the SMN, CEN, LN, and VN among adolescents exposed to SARS-CoV-2. Moreover, changes in rs-FC associated with PLEs existed in these adolescents despite the absence of clinical changes. Furthermore, inflammation response was correlated with alterations in FC within the triple network system.en-USCC BY 4.0 Deed (Attribution 4.0 International)COVID-19Psychosis pronenessNeuroimagingFunctional connectivityAdolescentInflammation markersBrain networksThe effect of SARS-CoV-2 virus on resting-state functional connectivity during adolescence: Investigating brain correlates of psychotic-like experiences and SARS-CoV-2 related inflammation responseArticle10.1016/j.pscychresns.2023.1117461872-7506