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<p>Several disrupted metabolic pathways contributed to the development of Parkinson’s disease (PD). Progressive death of dopamine (DA) neurons in the substantia nigra pars compacta, abnormal aggregation of α-synuclein fibrils, and inflammation of the neural system are the hallmarks of PD. The kynurenine pathway (KP) becomes disrupted, and excitotoxic branches are activated by elevated levels of central inflammatory regulators in PD. This leads to a significant reduction in the neural protective metabolite, kynurenic acid (KYNA), and an increase in the neurotoxic metabolite, quinolinic acid (QUIN), which together promote overstimulation and heightened immune responses, both closely related to the progression and onset of PD. KP enzyme modulators, precursor-based therapies, and KYNA analogs may provide a novel way to treat PD. KP components may also serve as new prognostic indicators and therapeutic targets for PD. Finding precise biomarkers for early screening, involving preclinical and prodromal stages, is essential for improving therapeutic intervention and care at the onset of PD. The current review provides an updated analysis of KP study results related to PD. Additionally, the review highlights the need for expanded biomarker research, which could help establish new therapeutic approaches for PD.</p> Graphical abstract <p></p>

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Kynurenine pathway in Parkinson’s disease: pathophysiological roles and therapeutic interventions

  • 期刊论文

  • 发表日期：

    2025年11月27日

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  • Aganta Chakraborty,
  • Priya Chaudhary,
  • Joy Das,
  • Utpal Bhui,
  • Khadga Raj Aran,
  • Md Sadique Hussain,
  • Sumel Ashique,
  • Biplab Debnath

摘要

Several disrupted metabolic pathways contributed to the development of Parkinson’s disease (PD). Progressive death of dopamine (DA) neurons in the substantia nigra pars compacta, abnormal aggregation of α-synuclein fibrils, and inflammation of the neural system are the hallmarks of PD. The kynurenine pathway (KP) becomes disrupted, and excitotoxic branches are activated by elevated levels of central inflammatory regulators in PD. This leads to a significant reduction in the neural protective metabolite, kynurenic acid (KYNA), and an increase in the neurotoxic metabolite, quinolinic acid (QUIN), which together promote overstimulation and heightened immune responses, both closely related to the progression and onset of PD. KP enzyme modulators, precursor-based therapies, and KYNA analogs may provide a novel way to treat PD. KP components may also serve as new prognostic indicators and therapeutic targets for PD. Finding precise biomarkers for early screening, involving preclinical and prodromal stages, is essential for improving therapeutic intervention and care at the onset of PD. The current review provides an updated analysis of KP study results related to PD. Additionally, the review highlights the need for expanded biomarker research, which could help establish new therapeutic approaches for PD.

Graphical abstract