Alzheimer disease and neuroinflammation

  • Patrick L. McGeer
  • E. G. McGeer
  • K. Yasojima
Conference paper


It is now generally accepted that the lesions of Alzheimer disease (AD) are associated with a host of inflammatory molecules, including complement proteins, as well as with many activated microglia. Most inflammatory components are synthesized by brain cells. In order to estimate the intensity of the inflammatory reaction, we have measured the levels of the mRNAs for complement proteins, two complement regulators (CD59 and CI inhibitors), an acute phase reactant (C-reactive protein, CRP) and two microglial markers, (HLA-DR and CDllb), in normal and AD brain. The mRNAs for inflammatory mediators are markedly upregulated in AD tissue while those of the complement inhibitors are almost unchanged. The upregulations for CRP and CDllb in AD hippocampus are comparable to those in osteoarthritic joints. This lends further support to the hypothesis that chronic inflammation may be causing neuronal death in AD.


Alzheimer Disease Acute Phase Reactant Complement Protein Complement Regulator Neurobiol Aging 
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Copyright information

© Springer-Verlag 2000

Authors and Affiliations

  • Patrick L. McGeer
    • 2
  • E. G. McGeer
    • 1
  • K. Yasojima
    • 1
  1. 1.Kinsmen Laboratory of Neurological ResearchDepartment of Psychiatry, University of British ColumbiaVancouverCanada
  2. 2.Kinsmen Laboratory of Neurological ResearchUniversity of British ColumbiaVancouverCanada

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