| First Author | Park SA | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 478 |
| Issue | 1 | Pages | 286-292 |
| PubMed ID | 27425247 | Mgi Jnum | J:238664 |
| Mgi Id | MGI:5823329 | Doi | 10.1016/j.bbrc.2016.07.015 |
| Citation | Park SA, et al. (2016) Deficiency in either COX-1 or COX-2 genes does not affect amyloid beta protein burden in amyloid precursor protein transgenic mice. Biochem Biophys Res Commun 478(1):286-92 |
| abstractText | Epidemiologic studies indicate that chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with a lower risk for developing Alzheimer's disease (AD). Because the primary mode of action of NSAIDs is to inhibit cyclooxygenase (COX) activity, it has been proposed that perturbed activity of COX-1 or COX-2 contributes to AD pathogenesis. To test the role of COX-1 or COX-2 in amyloid deposition and amyloid-associated inflammatory changes, we examined amyloid precursor protein (APP) transgenic mice in the context of either COX-1 or COX-2 deficiency. Our studies showed that loss of either COX-1 or COX-2 gene did not alter amyloid burden in brains of the APP transgenic mice. However, one marker of microglial activation (CD45) was decreased in brains of COX-1 deficient/APP animals and showed a strong trend in reduction in COX-2 deficient/APP animals. These results suggest that COX activity and amyloid deposition in brain are likely independent processes. Further, if NSAIDs do causally reduce the risks of AD, then our findings indicate that the mechanisms are likely not due primarily to their inhibition on COX or gamma-secretase modulation activity, the latter reported recently after acute dosing of ibuprofen in humans and nonhuman primates. |
