Year: 2025 | Month: May | Volume: 12 | Issue: 5 | Pages: 646-655
DOI: https://doi.org/10.52403/ijrr.20250568
Biochemical Correlation Between KYNA and Glutamate Concentrations in Schizophrenia: Evidence from Clinical Serum Analysis
Mutiara Anissa1,2, Afriwardi3, Yaslinda Yaunin4, Rauza Sukma Rita5
1Doctoral Program in Biomedical, Faculty of Medicine, Universitas Andalas, Padang, Indonesia.
2Department of Psychiatry, Faculty of Medicine, Universitas Baiturrahmah, Padang, Indonesia.
3Department of Physiology, Faculty of Medicine, Universitas Andalas, Padang, Indonesia.
4Department of Psychiatry, Faculty of Medicine, Universitas Andalas, Padang Indonesia.
5Department of Biochemistry, Faculty of Medicine, Universitas Andalas, Padang Indonesia.
Corresponding Author: Afriwardi
ABSTRACT
Background: Different from other neuropsychiatric diseases, schizophrenia is defined by negative, cognitive, and psychotic symptoms. Recent neurobiological theories link glutamatergic dysfunction to kynurenic acid (KYNA), a metabolite of tryptophan. The relationship between KYNA and glutamate suggests pathogenic processes including excitotoxicity and NMDA receptor hypofunction. This study assessed the relationship between serum concentrations of KYNA and glutamate in individuals diagnosed with schizophrenia.
Methods: This study was a cross-sectional observational investigation involving 99 individuals with schizophrenia treated at Prof. Dr. HB Saanin Psychiatric Hospital in Padang, Indonesia. Serum levels of KYNA and glutamate were quantified via ELISA. The statistical analysis encompassed univariate distribution and Spearman's correlation test.
Results: The median KYNA concentration was 14.6 nmol/L (IQR: 12.3–19.5), and the median glutamate concentration was 10.5 μg/mL (IQR: 9.2–12.5), both significantly higher relative to normative values. A robust positive connection was identified between KYNA and Glutamate Concentrations s (Spearman r = 0.701; p < 0.001).
Conclusion: This study demonstrates a strong positive association between glutamate and KYNA in schizophrenia, suggesting that they may serve ase interacting neurochemical indicators. These findings corroborate the significance of KYNA–glutamate dysregulation in the pathogenesis of schizophrenia and propose the kynurenine pathway as a viable target for prospective treatment approaches.
Keywords: schizophrenia, glutamate, kynurenic acid
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