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The pentraxins: possible role in Alzheimer's disease and other innate inflammatory diseases
E G McGeer1, K Yasojima, C Schwab
1Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, V6T 1Z3, Vancouver, B.C., Canada. mcgeer@interchange.ubc.ca
Abstract:
Two short pentraxins, C-reactive protein and amyloid P, are found in association with the senile plaques and neurofibrillary tangles of Alzheimer disease (AD). Formerly thought to be made primarily if not solely in liver, recent work has shown that they are made not only in the brain but in other tissues such as heart and arteries. Their synthesis is markedly upregulated in affected brain regions in AD. Since they are known to activate the complement cascade in an antibody-independent fashion and chronic activation can cause destruction of host tissue, these pentraxins may be important initiators of an autodestructive process. As such, they may be prime targets for therapeutic intervention.
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