Preliminary animal and human data suggest that estrogens may be protective against Alzheimer's disease in women. In a population-based case-control study at Group Health Cooperative of Puget Sound, Seattle, Washington, the authors compared the exposure of estrogen replacement therapy of 107 female Alzheimer's disease cases with 120 age- and sex-matched controls by using computerized pharmacy data. The cases were obtained from the Alzheimer's Disease Patient Registry of the University of Washington, Seattle, Washington, which is based on the enumerated health plan population from 1987 to 1992. Newly recognized cases of probable Alzheimer's disease according to standardized diagnostic criteria were ascertained, evaluated, and enrolled in the Registry. The controls were selected from the same defined population by stratified random sampling. When the authors applied logistic regression, ever use of estrogens did not show an association with Alzheimer's disease (adjusted odds ratio = 1.1, 95 percent confidence interval 0.6-1.8). Oral and vaginal estrogens yielded similar results. In conclusion, this study provides no evidence that estrogen replacement therapy has an impact on the risk of Alzheimer's disease in women.
We investigated whether cigarette smoking is negatively associated with Alzheimer's disease (AD) in a population-based, frequency-matched, case-control study of 152 AD patients and 180 controls. Ever having smoked was associated with lower risk of AD (adjusted odds ratio = 0.61; 95% confidence interval: 0.37-0.99). Additional multivariate analyses demonstrated that education and history of hypertension modified this association. The direction of the modification was for higher education level and history of hypertension to further reduce the risk. The "dose-response" pattern showed the greatest risk reduction among those who smoked least and suggests a biologic mechanism of a dose-dependent up-regulation of nicotinic (cholinergic) brain receptors. These data, although consistent with current opinion about pathophysiology of AD, do not suggest smoking should be used as a preventive strategy for AD.
When AD cases were followed from first diagnosis to death, the causes of death varied by level of cognitive impairment. Illnesses potentially amenable to treatment caused death at all levels of disease, but more so early in the course of AD. Cognitive impairment may make patients less able to recognize and report symptoms of medical problems, thereby complicating efforts to intervene.
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