McGeer P L [a]. McGeer E G. Yasojima K.
Alzheimer disease and neuroinflammation, Journal of Neural Transmission :53-57.
Abstract
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 C1 inhibitors), an
acute phase reactant (C-reactive protein, CRP) and two microglial markers,
(HLA-DR and CD11b), 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 CD11b 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.
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