Original ArticleNonsteroidal Anti-Inflammatory Drug Use and Alzheimer's Disease: A Case-Control Study in Rochester, Minnesota, 1980 Through 1984
Section snippets
Cases of AD and Control Subjects
During the performance of ongoing studies of dementing illness in Rochester, Minnesota, we identified persons with the onset of AD during the years 1980 through 1984.8 Health-care providers in Rochester are limited in number, and each provides diagnostic information and clinical details for the Rochester Epidemiology Project at Mayo Clinic Rochester.7 Although some cases of AD may not come to medical and diagnostic attention, we believe that scenario to be uncommon because more than 95% of the
Results
Among the 302 incident cases of AD with onset during the years 1980 through 1984 in Rochester, Minnesota, 152 (50%) had documentation of use of either prescription or nonprescription NASIDs during the 2-year time window described. Similarly, 161 of the 302 age- and sex-matched control subjects (53%) had evidence of exposure to either prescription or nonprescription NASIDs during the 2-year window described.
As noted in the Methods section, three categories of exposure to NASIDs were used in this
Discussion
Our findings failed to demonstrate a significant inverse association between use of NSAIDs and AD. Nevertheless, the point estimates of the OR were less than unity except for exposure to aspirin in men and prescription NSAIDs in women, a finding that could be interpreted as suggestive of a protective effect. The results of two studies 3,4 strongly suggest that NSAIDs are protective for AD. One of them, the Canadian Study of Health and Aging,4 used prevalent cases with age- and group-matched
Conclusion
Although our current study failed to confirm a protective effect of use of NSAIDs on AD, results from earlier investigations were equivocal as well Additional longitudinal studies of the use of NSAIDs in other populations are needed for further assessment of this potential association.
References (27)
- et al.
Detection of the membrane inhibitor of reactive lysis (CD59) in diseased neurons of Alzheimer brain
Brain Res
(1991) - et al.
Rheumatoid arthritis and susceptibility to Alzheimer's disease [letter]
Lancet
(1991) - et al.
Influence of reduction of serum lipids on prognosis of coronary heart-disease: a five-year study using oestrogen
Lancet
(1961) - et al.
The Rochester Coronary Heart Disease Project: effect of cigarette smoking, hypertension, diabetes, and steroidal estrogen use on coronary heart disease among 40- to 59-year-old women, 1960 through 1982
Mayo Clin Proc
(1989) - et al.
Clinical trial of indomethacin In Alzheimer's disease
Neurology
(1993) - et al.
Inverse association of anti-inflammatory treatments and Alzheimer's disease: initial results of a co-twin control study
Neurology
(1994) - et al.
Nonsteroidal anti-inflammatory drugs in Alzheimer's disease
Neurology
(1995) The Canadian Study of Health and Aging: risk factors for Alzheimer's disease in Canada
Neurology
(1994)- et al.
Risk of Alzheimer's disease and duration of NSAID use
Neurology
(1997) - et al.
The patient record in epidemiology
Sei Am
(1981 oct)
Is the incidence of dementing illness changing? A 25-year time trend study in Rochester, Minnesota (1960-1984)
Neurology
Criteria for onset critically influence the estimation of familial risk in Alzheimer's disease
Genet Epidemiol
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This study was supported in part by Research Grants AR 30582, NS 17750, AG 06786, and AG 08031 from the National Institutes of Health, Public Health Service.