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

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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, Zinger, Anna, Herrero, Maria Trinidad, Guillemin, Gilles J.·2017·Progress in Neurobiology

DOI 10.1016/j.pneurobio.2015.12.009

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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.

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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.
ORCID: Lim, Chai K.
Braidy, Nady
Estrada, Cristina
Costa, Cristina
Bessede, Alban
Guillemin, Gilles J.
Venue: Progress in Neurobiology
Publisher: Elsevier BV
Published: 2017-08
Volume: 155
Pages: 76-95
ISSN: 0301-0082 (ISSN-L)
DOI: 10.1016/j.pneurobio.2015.12.009
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
FWCI: 0.82
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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 › Clinical 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

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

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