Neuroinflammation Mediated by IL-1β Increases Susceptibility of Dopamine Neurons to Degeneration in an Animal Model of Parkinson's Disease

DSpace/Manakin Repository

Neuroinflammation Mediated by IL-1β Increases Susceptibility of Dopamine Neurons to Degeneration in an Animal Model of Parkinson's Disease

Citable link to this page

. . . . . .

Title: Neuroinflammation Mediated by IL-1β Increases Susceptibility of Dopamine Neurons to Degeneration in an Animal Model of Parkinson's Disease
Author: Koprich, James B; Reske-Nielsen, Casper; Mithal, Prabhakar; Isacson, Ole Stefan

Note: Order does not necessarily reflect citation order of authors.

Citation: Koprich, James B., Casper Reske-Nielsen, Prabhakar Mithal, and Ole Isacson. 2008. Neuroinflammation mediated by IL-1β increases susceptibility of dopamine neurons to degeneration in an animal model of Parkinson's disease. Journal of Neuroinflammation 5: 8.
Full Text & Related Files:
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.
Published Version: doi://10.1186/1742-2094-5-8
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2292163/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:5347091

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters