Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease: A review of 17 epidemiologic studies
Abstract
Alzheimer's disease (AD) lesions are characterized by the presence of numerous inflammatory proteins. This has led to the hypothesis that brain inflammation is a cause of neuronal injury in AD and that anti-inflammatory drugs may act as protective agents. Seventeen epidemiologic studies from nine different countries have now been published in which arthritis, a major indication for the use of anti-inflammatory drugs, or anti-inflammatory drugs themselves have been considered as risk factors for AD. Both factors appear to be associated with a reduced prevalence of AD. The small size of most studies has limited their individual statistical significance, but similarities in design have made it possible to evaluate combined results. We have used established methods of statistical meta-analysis to estimate the overall chance of individuals exposed to arthritis or anti-inflammatory drugs developing AD as compared with the general population. Seven case-control studies with arthritis as the risk factor yielded an overall odds ratio of 0.556 (p < 0.0001), while four case-control studies with steroids yielded odds ratios of 0.656 (p = 0.049) and three case-control studies with nonsteroidal anti-inflammatory drugs (NSAIDs) yielded an odds ratio of 0.496 (p = 0.0002). When NSAIDs and steroids were combined into a single category of anti-inflammatory drugs, the odds ratio was 0.556 (p < 0.0001). Population-based studies were less similar in design than case-control studies, complicating…
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Long-term treatment with NSAIDs reduced the risk for AD, delayed disease onset, and slowed cognitive decline.
“The recognition that a robust inflammatory response contributes to AD also fuelled the discovery that long-term treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) reduced the risk for AD, delayed disease onset, and slowed cognitive decline (McGeer et al., 1996;Stewart et al., 1997;in t' in t'Veld et al., 2001).”
From PPARγ/RXRα-Induced and CD36-Mediated Microglial Amyloid-β Phagocytosis Results in Cognitive Improvement in Amyloid Precursor Protein/Presenilin 1 Mice (2012) · cites this paper as McGeer et al., 1996
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- Authors
- McGeer, P. L., Schulzer, M., & McGeer, E. G.
- Affiliations
- University of British Columbia (CA)
- ORCID
- McGeer, Patrick L.
- Venue
- Neurology
- Published
- 1996-08
- Volume
- 47
- Issue
- 2
- Pages
- 425-432
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2068477037
- Cited by
- 1,367
- References
- 1
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 14 · 2023: 16 · 2022: 25 · 2021: 34 · 2020: 24 · 2019: 21 · 2018: 26 · 2017: 37 · 2016: 41 · 2015: 34 · 2014: 34 · 2013: 36 · 2012: 44
- FWCI
- 9.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, arthritis, anti-inflammatory agents, nonsteroidal anti-inflammatory drugs, corticosteroids, neuroinflammation, neuroprotection, risk factors, rheumatoid arthritis, disease prevalence
- MeSH terms
- Alzheimer Disease, Anti-Inflammatory Agents, Arthritis, Humans, Risk Factors, Case-Control Studies
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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