The involvement of neuroinflammation and Kynurenine pathway in Parkinson's disease

Anna Zinger, Carlos Barcia, Maria Trinidad Herrero, Gilles J. Guillemin*

*Corresponding author for this work

Research output: Contribution to journalReview article

49 Citations (Scopus)
29 Downloads (Pure)

Abstract

Parkinsons disease (PD) is a common neurodegenerative disorder characterised by loss of dopaminergic neurons and localized neuroinflammation occurring in the midbrain several years before the actual onset of symptoms. Activated microglia themselves release a large number of inflammatory mediators thus perpetuating neuroinflammation and neurotoxicity. The Kynurenine pathway (KP), the main catabolic pathway for tryptophan, is one of the major regulators of the immune response and may also be implicated in the inflammatory response in parkinsonism. The KP generates several neuroactive compounds and therefore has either a neurotoxic or neuroprotective effect. Several of these molecules produced by microglia can activate the N-methyl-D-aspartate (NMDA) receptor-signalling pathway, leading to an excitotoxic 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 pharmacological modulation of the KP will represent a new therapeutic strategy for PD.

Original languageEnglish
Article number716859
Pages (from-to)1-11
Number of pages11
JournalParkinson's Disease
Volume2011
DOIs
Publication statusPublished - Jan 2011
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2011. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

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