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)].
- Animal model
- Nonsteroidal anti-inflammatory drug
- Oxidative stress
ASJC Scopus subject areas
- Clinical Neurology
- Immunology and Allergy
Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease. / Quinn, Joseph; Montine, Thomas; Morrow, Jason; Woodward, William; Kulhanek, Doris; Eckenstein, Felix.In: Journal of Neuroimmunology, Vol. 137, No. 1-2, 04.2003, p. 32-41.
Research output: Contribution to journal › Article