Complement activation in the Parkinson's disease substantia nigra: an immunocytochemical study
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Complement activation in the Parkinson's disease substantia nigra: an immunocytochemical study David A Loeffler*1, Dianne M Camp1 and Stephanie B Conant1,2 Address: 1Division of Neurology, William Beaumont Hospital Research Institute, Royal Oak, MI 48073, USA and 2Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA Email: David A Loeffler* - DLoeffler@beaumont.edu; Dianne M Camp - DCamp@beaumont.edu; Stephanie B Conant - stephanie.b.conant@vanderbilt.edu * Corresponding author
Published: 19 October 2006 Journal of Neuroinflammation 2006, 3:29
doi:10.1186/1742-2094-3-29
Received: 04 August 2006 Accepted: 19 October 2006
This article is available from: http://www.jneuroinflammation.com/content/3/1/29 © 2006 Loeffler et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Inflammatory processes are increased in the Parkinson's disease (PD) brain. The long-term use of nonsteroidal anti-inflammatory drugs has been associated, in retrospective studies, with decreased risk for PD, suggesting that inflammation may contribute to development of this disorder. The objective of this study was to determine the extent of complement activation, a major inflammatory mechanism, in PD. Methods: Substantia nigra specimens from young normal subjects (n = 11–13), aged normal subjects (n = 24–28), and subjects with PD (n = 19–20), Alzheimer's disease (AD; n = 12–13), and dementia with Lewy bodies (DLB; n = 9) were stained for iC3b and C9, representing early- and late-stage complement activation, respectively. Numbers of iC3b+, C9+, and total melanized neurons in each section were counted in a blinded fashion. Nonparametric analyses were used to evaluate differences between groups and to evaluate correlations between complement staining, numbers of melanized neurons, and the duration of PD. Results: Lewy bodies in both PD and DLB specimens stained for iC3b and C9. Staining was also prominent on melanized neurons. The percentage of iC3b+ neurons was significantly increased in PD vs. aged normal and AD specimens, and in young normal vs. aged normal specimens. C9 immunoreactivity was significantly increased in PD vs. AD specimens, but unlike iC3b, the increased C9 staining in PD and young normal specimens did not achieve statistical significance vs. aged normal specimens. iC3b and C9 staining in PD specimens was not correlated with the numbers of remaining melanized neurons, nor with the duration of PD. Conclusion: Complement activation occurs on Lewy bodies and melanized neurons in the PD substantia nigra. Early complement activation (iC3b) is increased on melanized neurons in PD vs. aged normal specimens, and late-stage complement activation (C9) also tends to increase.
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