Abstract
Introduction: Acute cerebrovascular disorders are a major contributor to adult disability. The underlying processes that contribute to their development include inflammation, excitotoxicity, oxidative stress, and dysregulation of the tryptophan–kynurenine pathway, which is essential for neuronal survival. However, the precise mechanisms and significance of these processes are not fully comprehended, and their influence on the efficacy of therapeutic approaches remains uncertain. The aim of this study is to investigate the role of the tryptophan-kynurenine metabolic pathway in the development of stroke and its potential as a biomarker and therapeutic target. Results and Conclusions: Tryptophan metabolism primarily occurs through the kynurenine pathway. Among its metabolites, kynurenine, kynurenic and choline acids are the most significant. Them have both neuroprotective and neurotoxic effects. Activation of the kynurenine pathway is linked to chronic inflammation, increasing the risk of cardiovascular and neurodegenerative conditions. Kynurenic and choline acids regulate N-methyl-D-aspartate receptor activity and oxidative stress. The increased production of choline and 3-hydroxyanthranilic acid due to oxidative stress is a major mechanism of neuronal damage under ischemic. The regulation of the balance between the neuroprotective and neurotoxic properties of metabolites produced by the kynurenine pathway is essential for normal brain function.