SynthesisMolecular and cellular biochemistry2026
Investigating the role of the kynurenine pathway in traumatic brain injury: a systematic review.
Synthesis in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- The role of the kynurenine pathway in the pathogenesis of pain and affective disorders after traumatic brain injury.Brain, behavior, & immunity - health · 2026Review
- A Novel snoRNA, Gm24418 Attenuates Inflammation Injury After Acute TBI Through Regulating CCL2.Journal of inflammation research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
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.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.