Decreased serum levels of α‐synuclein in patients with schizophrenia and their unaffected siblings

Abstract

AbstractAimThe final common pathway in the etiopathogenesis of schizophrenia is suggested that there is a defect in the presynaptic terminal in dopaminergic transmission, in which α‐synuclein has an important role. Peripheral biomarker studies in schizophrenia have become crucial for better diagnoses, early interventions, and personalized therapies. This study aims to compare α‐synuclein levels in patients with schizophrenia and their unaffected siblings with healthy controls, as a potential peripheral biomarker for schizophrenia.MethodsThe quantifications of α‐synuclein serum concentrations were conducted by the ELISA method. PANSS and CGI‐S were used to analyse the severity of the symptoms of the subjects. Data were analysed by nonparametric tests and the Receiver Operating Curve (ROC) analysis.ResultsSixty‐two patients with schizophrenia (mean age: 34,8 ± 9,9, %64,5 male), their 56 unaffected siblings (mean age: 39,4 ± 11,5, %55,4 male) and 56 healthy controls (mean age: 36,2 ± 9,8, %64,3 male) were included. α‐synuclein levels were significantly lower in the patient (27,65 (12,61‐46,09) pg/ml) and the unaffected sibling groups (24,62 (15,60‐57,87) pg/ml) compared with healthy controls (45,58 (11,25‐108,30) pg/ml) (p < .001). According to the ROC analysis, the optimal cut‐off value for α‐synuclein levels in distinguishing the schizophrenia group from the control group was 42.20. The sensitivity of the measurement of serum α‐synuclein at this point was 93.5%, and the specificity was 60.7%.ConclusionOur study demonstrates that decreased levels of serum α‐synuclein may be utilized as a possible peripheral biomarker of familial risk for schizophrenia in both patients and their siblings.