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Journal of Neuroinflammation
Published in: Journal of Neuroinflammation 1/2008

Open Access 01-12-2008 | Research

Neuroinflammation mediated by IL-1β increases susceptibility of dopamine neurons to degeneration in an animal model of Parkinson's disease

Authors: James B Koprich, Casper Reske-Nielsen, Prabhakar Mithal, Ole Isacson

Published in: Journal of Neuroinflammation | Issue 1/2008

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Abstract

Background

The etiology of Parkinson's disease (PD) remains elusive despite identification of several genetic mutations. It is more likely that multiple factors converge to give rise to PD than any single cause. Here we report that inflammation can trigger degeneration of dopamine (DA) neurons in an animal model of Parkinson's disease.

Methods

We examined the effects of inflammation on the progressive 6-OHDA rat model of Parkinson's disease using immunohistochemistry, multiplex ELISA, and cell counting stereology.

Results

We show that a non-toxic dose of lipopolysaccharide (LPS) induced secretion of cytokines and predisposed DA neurons to be more vulnerable to a subsequent low dose of 6-hydroxydopamine. Alterations in cytokines, prominently an increase in interleukin-1beta (IL-1β), were identified as being potential mediators of this effect that was associated with activation of microglia. Administration of an interleukin-1 receptor antagonist resulted in significant reductions in tumor necrosis factor-α and interferon-γ and attenuated the augmented loss of DA neurons caused by the LPS-induced sensitization to dopaminergic degeneration.

Conclusion

These data provide insight into the etiology of PD and support a role for inflammation as a risk factor for the development of neurodegenerative disease.
Appendix
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Metadata
Title
Neuroinflammation mediated by IL-1β increases susceptibility of dopamine neurons to degeneration in an animal model of Parkinson's disease
Authors
James B Koprich
Casper Reske-Nielsen
Prabhakar Mithal
Ole Isacson
Publication date
01-12-2008
Publisher
BioMed Central
Published in
Journal of Neuroinflammation / Issue 1/2008
Electronic ISSN: 1742-2094
DOI
https://doi.org/10.1186/1742-2094-5-8

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