Cited by 159Tryptophan and brain disordersParkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration Mechanisms

Involvement of the kynurenine pathway in the pathogenesis of Parkinson's disease

Lim, Chai K., Fernández-Gomez, Francisco J., Braidy, Nady, Estrada, Cristina, Costa, Cristina, Costa, Silvia, Bessede, Alban, Fernandez-Villalba, Emiliano +3 more·2017·Progress in Neurobiology

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by loss of dopaminergic neurons and localized neuroinflammation occurring in the midbrain several years before the actual onset of symptoms. Neuroinflammation leads to microglia activation and release of a large number of proinflammatory mediators. The kynurenine pathway (KP) of tryptophan catabolism is one of the major regulators of the immune response and is also likely to be implicated in the inflammatory and neurotoxic events in Parkinsonism. Several neuroactive compounds are produced through the KP that can be either a neurotoxic, neuroprotective or immunomodulator. Among these metabolites kynurenic acid (KYNA), produced by astrocytes, is considered as neuroprotective whereas quinolinic acid (QUIN), released by activated microglia, can activate the N-methyl-d-aspartate (NMDA) receptor-signalling pathway, leading to excitotoxicity and amplify the inflammatory response. Previous studies have shown that NMDA antagonists can ease symptoms and exert a neuroprotective effect in PD both in vivo and in vitro. There are to date several lines of evidence linking some of the KP intermediates and the neuropathogenesis of PD. Moreover, it is likely that some of the KP metabolites could be used as prognostic biomarkers and that pharmacological modulators of the KP enzymes could represent a new therapeutic strategy for PD.

Integrity signals

Registry

Crossref · 10.1016/j.pneurobio.2015.12.009

Cites

270 of 270 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Lim, C. K., Fernández-Gomez, F. J., Braidy, N., Estrada, C., Costa, C., Costa, S., Bessede, A., Fernandez-Villalba, E., Zinger, A., Herrero, M. T., & Guillemin, G. J.
Affiliations
  • Macquarie University (AU)
  • UNSW Sydney (AU)
  • Instituto Murciano de Investigación Biosanitaria (ES)
  • Universidade Federal da Bahia (BR)
  • The University of Sydney (AU)
  • St Vincent's Hospital Sydney (AU)
Corresponding author
Guillemin, Gilles J.
Venue
Progress in Neurobiology
Publisher
Elsevier BV
Published
2017-08
Volume
155
Pages
76-95
ISSN
0301-0082 (ISSN-L)
OpenAlex
W2322232345
Cited by
159
References
270
Citations by year
2026: 8 · 2025: 19 · 2024: 19 · 2023: 14 · 2022: 17 · 2021: 22 · 2020: 19 · 2019: 22 · 2018: 6 · 2017: 10 · 2016: 3
FWCI
0.82
Type
journal article
Language
en
Open access
closed
Locations
  • Progress in Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Spanish Ministry of Science and Innovation (01293)
  • European Community’s Seventh Framework Programme (115009)
  • Australian Research Council
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Parkinson's disease, kynurenine pathway, tryptophan catabolism, neuroinflammation, microglial activation, kynurenic acid, quinolinic acid, NMDA receptor, excitotoxicity, dopaminergic neuron loss, neuroprotection, NMDA receptor antagonists, biomarkers, therapeutic target
MeSH terms
Animals, Humans, Kynurenine, Parkinson Disease

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review