Alzheimer disease and neuroinflammation.
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.
McGeer
P L
PL
Department of Psychiatry, University of British Columbia, Vancouver, Canada.
McGeer
E G
EG
Yasojima
K
K
D000544:Alzheimer Disease / Q000378:metabolism*; D015415:Biomarkers; D001921:Brain / Q000378:metabolism; D002097:C-Reactive Protein / Q000235:genetics; D003169:Complement Inactivator Proteins / Q000378:metabolism; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D016177:Macrophage-1 Antigen / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D017628:Microglia / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D015854:Up-Regulation
D015415:Biomarkers; D003169:Complement Inactivator Proteins; D006684:HLA-DR Antigens; D018836:Inflammation Mediators; D016177:Macrophage-1 Antigen; D012333:RNA, Messenger; D002097:C-Reactive Protein