| First Author | Quinn J | Year | 2003 |
| Journal | J Neuroimmunol | Volume | 137 |
| Issue | 1-2 | Pages | 32-41 |
| PubMed ID | 12667645 | Mgi Jnum | J:128812 |
| Mgi Id | MGI:3768044 | Doi | 10.1016/s0165-5728(03)00037-7 |
| Citation | Quinn J, et al. (2003) Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease. J Neuroimmunol 137(1-2):32-41 |
| abstractText | The hypothesis that inflammation and beta amyloid deposition are causally linked in Alzheimer's disease (AD) was tested in a transgenic mouse model. Untreated beta amyloid plaque-bearing Tg2576 mice did not differ from wild type animals in brain levels of most inflammatory mediators. Indomethacin treatment suppressed brain levels of prostaglandins by 90%, but reduced hippocampal beta amyloid by only 20%, with no effect on cortical beta amyloid. The discordant effects on beta amyloid and cyclooxygenase (COX) suggest that these effects of nonsteroidal anti-inflammatory drugs (NSAIDs) are not causally linked. Further evidence against a causal relationship is seen in an unexpected trend to lower levels of beta amyloid after an inflammatory stimulus [lipopolysaccharide (LPS)]. |
