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Publication : Induction of the complement component C1qB in brain of transgenic mice with neuronal overexpression of human cyclooxygenase-2.

First Author  Spielman L Year  2002
Journal  Acta Neuropathol Volume  103
Issue  2 Pages  157-62
PubMed ID  11810182 Mgi Jnum  J:100962
Mgi Id  MGI:3590104 Doi  10.1007/s004010100447
Citation  Spielman L, et al. (2002) Induction of the complement component C1qB in brain of transgenic mice with neuronal overexpression of human cyclooxygenase-2. Acta Neuropathol (Berl) 103(2):157-62
abstractText  We report that overexpression of human (h) cyclooxygenase-2 h(COX-2) in the brain of a transgenic mouse line leads to selective induction of endogenous complement component C1qB expression in neurons. No detectable induction of the C3 and C4 complement components in the brain was found. Chronic treatment of mice with the selective COX-2 inhibitor nimesulide reduced the hCOX-2-mediated induction of hippocampal C1qB mRNA expression. The data suggest that neuronal COX-2 expression may influence inflammatory responses in the brain, in part through modulation of complement gene expression. Because there is extensive evidence that C1q and other complement components are involved in Alzheimer's disease (AD) neurodegeneration, this study advances our understanding of the apparent benefits of COX-2 inhibition in AD.
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