C-reactive protein-like immunoreactivity in the neurofibrillary tangles of Alzheimer's disease

C-reactive protein-like immunoreactivity in the neurofibrillary tangles of Alzheimer's disease C-reactive protein (CRP) is a plasma acute-phase protein, normally not found in the brain. Previous studies have demonstrated the presence of CRP in the senile plaques of Alzheimer's disease (AD). In this study, the presence of CRP-like immunoreactivity in AD neurofibrillary tangles (NFT) was demonstrated following pre-treatment of tissue sections with formic acid. CRP-like immunoreactivity was observed in both extracellular and intracellular NFT and was co-localized with the NFT marker PHF-1 and the amyloid P component (AP). The CRP-like immunoreactive NFT were less numerous and more limited in their distribution than PHF-1 or AP-immunoreactive NFT. The present results further support an involvement of inflammatory processes in the etiology of AD. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

C-reactive protein-like immunoreactivity in the neurofibrillary tangles of Alzheimer's disease

Brain Research, Volume 749 (1) – Feb 21, 1997

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Publisher
Elsevier
Copyright
Copyright © 1997 Elsevier Ltd
ISSN
0006-8993
D.O.I.
10.1016/S0006-8993(96)01359-5
Publisher site
See Article on Publisher Site

Abstract

C-reactive protein (CRP) is a plasma acute-phase protein, normally not found in the brain. Previous studies have demonstrated the presence of CRP in the senile plaques of Alzheimer's disease (AD). In this study, the presence of CRP-like immunoreactivity in AD neurofibrillary tangles (NFT) was demonstrated following pre-treatment of tissue sections with formic acid. CRP-like immunoreactivity was observed in both extracellular and intracellular NFT and was co-localized with the NFT marker PHF-1 and the amyloid P component (AP). The CRP-like immunoreactive NFT were less numerous and more limited in their distribution than PHF-1 or AP-immunoreactive NFT. The present results further support an involvement of inflammatory processes in the etiology of AD.

Journal

Brain ResearchElsevier

Published: Feb 21, 1997

References

  • A case of familial, atypical Alzheimer's disease: immunohistochemical study of amyloid P-component
    Iseki, E.; Amano, N.; Matsuishi, T.; Yokoi, S.; Arai, N.; Yagishita, S.
  • The inflammatory response system of brain: implications of therapy of Alzheimer and other neurodegenerative diseases
    McGeer, P.L.; McGeer, E.G.

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