Protective effects of NSAIDs on the development of Alzheimer disease

Boston University School of Medicine, Clinical Epidemiology Research and Training Unit, 650 Albany St., Suite X200, Boston, MA 02118, USA.
Neurology (Impact Factor: 8.29). 05/2008; 70(19):1672-7. DOI: 10.1212/01.wnl.0000311269.57716.63
Source: PubMed


Nonsteroidal anti-inflammatory drugs (NSAIDs) may protect against Alzheimer disease (AD), but observational studies and trials have offered contradictory results. Prior studies have also been relatively short and small. We examined the effects on AD risk of NSAID use for >5 years and of NSAIDs that suppress formation of A beta (1-42) amyloid in a large health care database.
Cases were veterans aged 55 years and older with incident AD using the US Veterans Affairs Health Care system. Matched controls were drawn from the same population. NSAID exposure was categorized into seven time periods: no use, <or=1 year, >1 but <or=2 years, and so on. Using conditional logistic regression, adjusted for race and comorbidities, we tested the association between AD development and the use of 1) any NSAID, 2) any NSAID excluding nonacetylated salicylates, 3) each NSAID class, 4) each individual NSAID, and 5) A beta (1-42)-suppressing NSAIDs.
We identified 49,349 cases and 196,850 controls. Compared with no NSAID use, the adjusted odds ratios for AD among NSAID users decreased from 0.98 for <or=1 year of use (95% CI 0.95-1.00) to 0.76 for >5 years of use (0.68-0.85). For users of ibuprofen, it decreased from 1.03 (1.00-1.06) to 0.56 (0.42-0.75). Effects of other NSAID classes and individual NSAIDs were inconsistent. There was no difference between a group of A beta (1-42)-suppressing NSAIDs and others. Discussion: Long-term nonsteroidal anti-inflammatory drug (NSAID) use was protective against Alzheimer disease. Findings were clearest for ibuprofen. A beta (1-42)-suppressing NSAIDs did not differ from others.

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Available from: Steven C Vlad, Sep 28, 2015
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    • "Although mechanisms that cause AD are poorly understood, recent studies support the role of inflammation in hippocampal degeneration in AD. First, long-term use of nonsteroidal anti-inflammatory drugs has been shown to be protective for AD [7]. Second , activated astrocytes and microglia are seen in close association with amyloid plaques in the human ISSN 1387-2877/15/$35.00 "
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    • "Aging has been associated with an increasing neuroinflammatory process (Richwine et al., 2005; Ye and Johnson, 1999), and systemic inflammation may be associated with several pathologies, such as, coronary heart disease, diabetes, multiple sclerosis, Alzheimer's disease, and Parkinson's disease (Fito et al., 2007). However, anti-inflammatory therapies have shown mixed and discouraging results (Imbimbo et al., 2010; In t' Veld et al., 2001; Stewart et al., 1997; Vlad et al., 2008). Dietary strategies visibly influence inflammation, as related through both observational studies and controlled feeding trials in which subjects had limited food consumption (Giugliano et al., 2006; Harvie et al., 2011; Johnson et al., 2007; Mozaffarian et al., 2009). "
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    • "Epidemiological studies show a possible association between suppression of inflammation and reduced risk for AD (in t' Veld et al., 2001; Vlad et al., 2008). Therefore, drugs targeting neuroinflammation might provide benefits for the prevention and treatment of this devastating disease. "
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