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Parkinson’s Disease
Volume 2011, Article ID 716859, 11 pages
Review Article

The Involvement of Neuroinflammation and Kynurenine Pathway in Parkinson's Disease

1Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia
2Experimental and Clinical Neuroscience (NiCE-CIBERNED), Department of Human Anatomy and Psychobiology, School of Medicine, University of Murcia, Murcia, Spain
3St Vincent's Centre for Applied Medical Research, Darlinghurst, NSW 2010, Australia

Received 1 December 2010; Accepted 31 January 2011

Academic Editor: Heinz Reichmann

Copyright © 2011 Anna Zinger et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Parkinson’s 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.