ReviewInflammopharmacology2026
Kynurenine pathway in Parkinson's disease: pathophysiological roles and therapeutic interventions.
Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Bidirectional Mechanisms Linking Circadian Rhythm Disruption and Parkinson's Disease: Chronobiomarkers and Therapeutic Implications.International journal of molecular sciences · 2026Review
- From clinical phenotypes to molecular stratification: early differential diagnosis of four-repeat tauopathies.Frontiers in aging neuroscience · 2026Review
- Imaging biomarkers in neurodegenerative diseases: advances and challenges.Frontiers in aging neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
41298978What Socratic holds
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 Socratic graph.