Objective: The aim of the study was to evaluate the levels of peripheric biomarkers that have been associated with blood brain barrier (BBB) damage in healthy controls and two groups of patients with schizophrenia, those who received typical-atypical antipsychotics and those who received only atypical antipsychotics. Additionally, we sought relationships between these biomarkers and schizophrenia symptoms. Methods: This study was conducted with the inclusion of 41 healthy volunteers and 75 patients with schizophrenia. The biomarkers measured to evaluate BBB injury were as follows: spectrin breakdown product 145 (SBDP145), spectrin breakdown product 150 (SBDP150), ubiquitin carboxy terminal hydrolase L1 (UCHL1), ubiquitin ligase cullin-3 (cullin), occludin and claudin, which were measured via ELISA. Symptoms of patients with schizophrenia were evaluated with the Scale for the Assessment of Positive Symptoms (SAPS), Scale for the Assessment of Negative Symptoms, the Clinical Global Impression Scale (CGI), and the general assessment of functionality (GAF). Results: Compared to controls, SBDP145 (p = 0.022) and cullin (p = 0.046) levels were significantly higher in patients with schizophrenia receiving atypical antipsychotic treatment. SBDP150 levels were lower in the combination treatment group compared to the control group (p = 0.022). Claudin (p = 0.804), occludin (p = 0.058) and UCHL1 (p = 0.715) levels were similar among groups. In recipients of combination treatment, SBDP145 levels were found to be positively correlated with SAPS-total (r = 0.440, p = 0.036) and SAPS-delusions (r = 0.494, p = 0.017) scores. Conclusion The relationships demonstrated in this study indicate that more comprehensive research is needed to understand whether BBB defects contribute to clinical characteristics in patients with schizophrenia.

OBJECTIVE: α-synuclein, Nogo-A and Ubiquitin C-terminal hydrolase L1 (UCH-L1) have neuromodulatory roles for human brain. Therefore, abnormalities of these molecules are associated with neuropsychiatric disorders. Although some serum studies in the other disorders have been made, serum study of α-synuclein, Nogo-A and UCH-L1 is not present in patients with schizophrenia and healthy controls. Therefore, our aim was to compare serum levels of α-synuclein, Nogo-A and UCH-L1 of the patients with schizophrenia and healthy controls. METHODS: Forty-four patients with schizophrenia who is followed by psychotic disorders unit, and 40 healthy control were included in this study. Socio-demographic form and Positive and Negative Syndrome Scale (PANSS) was applied to patients, and sociodemographic form was applied to control group. Fasting bloods were collected and the serum levels of α-synuclein, Nogo-A and UCH-L1 were measured by ELISA method. RESULTS: Serum α-synuclein [patient: 12.73 (5.18–31.84) ng/mL; control: 41.77 (15.12–66.98) ng/mL], Nogo-A [patient: 33.58 (3.09–77.26) ng/mL; control: 286.05 (136.56–346.82) ng/mL] and UCH-L1 [patient: 5.26 (1.64–10.87) ng/mL; control: 20.48 (11.01–20.81) ng/mL] levels of the patients with schizophrenia were significianly lower than healthy controls (p<0.001). CONCLUSION: Our study results added new evidence for explaining the etiopathogenesis of schizophrenia on the basis of neurochemical markers.
Biomarkers ; Brain ; Enzyme-Linked Immunosorbent Assay ; Fasting ; Humans ; Methods ; Psychotic Disorders ; Schizophrenia* ; Ubiquitin Thiolesterase