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 pro teins, as well as with many activated microglia. Most inflammatory componen ts are synthesized by brain cells. In order to estimate the intensity of th e inflammatory reaction, we have measured the levels of the mRNAs for compl ement proteins, two complement regulators (CD59 and C1 inhibitors), an acut e phase reactant (C-reactive protein, CRP) and two microglial markers, (HLA -DR and CD11b), in normal and AD brain. The mRNAs for inflammatory mediator s are markedly upregulated in AD tissue while those of the complement inhib itors are almost unchanged. The upregulations for CRP and CD11b in AD hippo campus are comparable to those in osteoarthritic joints. This lends further support to the hypothesis that chronic inflammation may be causing neurona l death in AD.