Dysregulation of Triptophan Hydroxylation and Oxidation Path in Schizophrenia and Effects on Cognitive Functions and Clinical Symptoms

Abstract

Abstract Objective In our study, we aimed to examine the relationship between tryptophan kynurenine pathway and schizophrenia symptom clusters and cognitive functions.Method 46 patients in remission and 42 controls of the same gender, age and education level were included in the study. MCCB was applied to all participants to evaluate cognitive functions. Serotonin level to evaluate the tryptophan synthesis pathway; blood KYNA level to assess impairment; The tryptophan degradation enzyme IDO and some inflammation biomarkers predicted to increase its activity were measured. The levels of hsCRP and neopterin, which are biomarkers of inflammation, were examined.Results We found KYNA and serotonin serum levels were significantly lower in the patient group than in the control group. IDO was expressed at a lower level in the patient group compared to the control group, the difference between the groups was not statistically significant. Neopterin level in the patient group was found lower than the control group, this difference was not statistically significant. The cognitive performance of patients in the total MCCB scores and the scores of all subscales were significantly lower than those in healthy controls.Conclusion A Tryptophan oxidation pathway could be a valuable candidate for future therapeutic research for the treatment of neurodegenerative diseases such as schizophrenia. With our study, we aimed to contribute to the literature in this area where the findings are limited.