Journal
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
Volume 9, Issue 2, Pages 140-148Publisher
BENTHAM SCIENCE PUBL
DOI: 10.2174/187152710791011991
Keywords
Alzheimer's disease; cyclooxygenases; non-steroidal anti-inflammatory drugs; docosahexaenoic acid; curcumin
Categories
Funding
- NCCAM NIH [R01AT3008]
- NIH NIA [RO1 AG13471]
- VA Merit
- Mary S. Easton Alzheimer's Center
- Easton Drug Discovery Consortium
- [U01AG28583]
- [AG021975]
Ask authors/readers for more resources
Alzheimer's disease (AD) is accompanied by an activation of the innate immune system, and many epidemiological studies have shown reduced risk for dementia or AD associated with chronic consumption of non-steroidal anti-inflammatory drugs (NSAIDS). These observations led to animal model studies to test the hypothesis that NSAIDs can be disease-modifying for some aspects of AD pathogenesis. NSAIDS cannot only suppress inflammatory targets, which could contribute to neuroprotection, they also slow amyloid deposition by mechanisms that remain unclear. Several large clinical trials with NSAID therapies with AD subjects have failed, and cyclooxygenase-2 does not appear to be a useful target for disease modifying therapy. However, there may be apolipoprotein E E4 pharmacogenomic effects and a real but delayed positive signal in a large primary prevention trial with naproxen. This encourages researchers to re-address possible mechanisms for a stage-dependent NSAID efficacy, the subject of this review.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available