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42-lowering NSAIDs for prevention of Alzheimer dementia in six pooled cohort studies
stbye MD, PhD,
From Johns Hopkins Bloomberg School of Public Health (C.A.S., P.P.Z.), Baltimore, MD; Cedars-Sinai Medical Center, Los Angeles, CA (C.A.S.); Boston University School of Medicine (R.C.G., P.A.W.), MA; Boston University School of Public Health (R.C.G., A.S.B.), MA; VA Puget Sound Health Care System and University of Washington (J.C.S.B.), Seattle; Duke University Medical Center (T.., K.A.W.-B.), Durham, NC; Duke-NUS Graduate Medical School Singapore (T..); University of California Irvine School of Medicine (M.M.C., C.H.K.); Oregon State University College of Health and Human Sciences (H.H.D.), Corvallis; University of Pittsburgh Graduate School of Public Health (H.H.D.), PA; University of Pittsburgh School of Medicine (M.G., L.H.K.), PA; University of Washington School of Medicine and School of Public Health (B.M.P.), Seattle; and Intramural Research Program, National Institute on Aging (S.M.R., A.B.Z.), Baltimore, MD.
* To whom correspondence should be addressed. E-mail: pzandi{at}jhsph.edu.
Introduction: Observational studies show reduced incidence of Alzheimer dementia (AD) in users of nonsteroidal anti-inflammatory drugs (NSAIDs). One hypothesis holds that the subset of NSAIDs known as selective A
42-lowering agents (SALAs) is responsible for this apparent reduction in AD risk.
Methods: We pooled individual-level data from six prospective studies to obtain a sufficient sample to examine AD risk in users of SALA vs non-SALA NSAIDs.
Results: Of 13,499 initially dementia-free participants (70,863 person-years), 820 developed incident AD. Users of NSAIDs (29.6%) showed reduced risk of AD (adjusted hazard ratio [aHR] 0.77, 95% CI 0.65–0.91). The point estimates were similar for SALAs (aHR 0.87, CI 0.72–1.04) and non-SALAs (aHR 0.75, CI 0.56–1.01). Because 573 NSAID users (14.5%) reported taking both a SALA and non-SALA, we examined their use alone and in combination. Resulting aHRs were 0.82 (CI 0.67–0.99) for SALA only, 0.60 (CI 0.40–0.90) for non-SALA only, and 0.87 (CI 0.57–1.33) for both NSAIDs (Wald test for differences, p = 0.32). The 40.7% of participants who used aspirin also showed reduced risk of AD, even when they used no other NSAIDs (aHR 0.78, CI 0.66–0.92). By contrast, there was no association with use of acetaminophen (aHR 0.93, CI 0.76–1.13).
Conclusions: In this pooled dataset, nonsteroidal anti-inflammatory drug (NSAID) use reduced the risk of Alzheimer dementia (AD). However, there was no apparent advantage in AD risk reduction for the subset of NSAIDs shown to selectively lower A42, suggesting that all conventional NSAIDs including aspirin have a similar protective effect in humans.
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