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<p>Traumatic brain injury (TBI) disrupts normal brain function through inflammatory cascades that may persist for months or years. This review aimed to gather the evidence regarding kynurenine pathway (KP) dysregulation following TBI and to examine how altered KP metabolites correlate with clinical outcomes. We systematically identified relevant human studies in PubMed and Lilacs databases using descriptors linked to TBI and KP metabolites. We included original research in English, Portuguese, or Spanish with no publication date restriction. We extracted data on participant characteristics, TBI severity, metabolite levels, and clinical endpoints. We appraised risk of bias using standardized checklists for cohort and cross‑sectional designs. Twelve studies met inclusion criteria. TBI increases circulating levels of quinolinic acid (QUIN), with higher QUIN linked to mortality in severe TBI and worse mood or cognitive sequelae in mild TBI. Kynurenine and kynurenic acid changes varied across cohorts, reflecting the complexity of post-injury inflammatory processes. TBI can disrupt KP metabolism and increased levels of QUIN are associated with poor neurological outcomes. Future research should define the dynamics of KP metabolite production over time and assess whether targeted interventions can lessen neurotoxic load. Post‑injury neuroinflammation remains a critical focus for potential therapeutic intervention strategies.</p>

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Investigating the role of the kynurenine pathway in traumatic brain injury: a systematic review

  • 期刊论文

  • 发表日期：

    2025年11月3日

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  • João Luís Vieira Monteiro de Barros,
  • Maíra Glória de Freitas Cardoso,
  • Thiago Martins da Silva,
  • Vivian Vasconcelos Costa,
  • Antônio Lúcio Teixeira,
  • Aline Silva de Miranda

摘要

Traumatic brain injury (TBI) disrupts normal brain function through inflammatory cascades that may persist for months or years. This review aimed to gather the evidence regarding kynurenine pathway (KP) dysregulation following TBI and to examine how altered KP metabolites correlate with clinical outcomes. We systematically identified relevant human studies in PubMed and Lilacs databases using descriptors linked to TBI and KP metabolites. We included original research in English, Portuguese, or Spanish with no publication date restriction. We extracted data on participant characteristics, TBI severity, metabolite levels, and clinical endpoints. We appraised risk of bias using standardized checklists for cohort and cross‑sectional designs. Twelve studies met inclusion criteria. TBI increases circulating levels of quinolinic acid (QUIN), with higher QUIN linked to mortality in severe TBI and worse mood or cognitive sequelae in mild TBI. Kynurenine and kynurenic acid changes varied across cohorts, reflecting the complexity of post-injury inflammatory processes. TBI can disrupt KP metabolism and increased levels of QUIN are associated with poor neurological outcomes. Future research should define the dynamics of KP metabolite production over time and assess whether targeted interventions can lessen neurotoxic load. Post‑injury neuroinflammation remains a critical focus for potential therapeutic intervention strategies.