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To the Editor: – A previous study by Apple1 has suggested that smoking may decrease a person's risk of developing Alzheimer's disease. Our data were obtained either from patients seen at the Division of Geriatric Psychiatry of the Department of Psychiatry and Human Behavior at St. Louis University Medical Center or from persons registered with the St. Louis University Medical Center/Alzheimer's Disease and Related Disorders Association Brain Bank. A smoking history, including use of smokeless tobacco, was obtained for these patients by phone interviews of surrogate respondents. French et al2 showed that there was no significant prevalence, incidence bias, or recall bias when obtaining information from a surrogate respondent. Control data were collected from nondemented medical patients matched on average for age, sex, and race. It appears that this study includes the largest group of Alzheimer's disease patients studied with respect to smoking. Of the 144 Alzheimer's patients, 44 (31%) smoked tobacco compared to 55 (57%) of the 96 people in the control group (X2 = 16.4, P < .01) (see table). Of the 44 with Alzheimer's disease, 22 (50%) quit smoking prior to diagnosis of Alzheimer's disease. In the control group, 36 (65%) of the 55 stopped smoking prior to this survey. Our findings also indicate that people who used tobacco developed Alzheimer's disease an average of two years earlier, but these findings were not statistically significant (χ2 = 2.10). Our results confirm the findings of Apple1 suggesting smoking may decrease a person's risk of developing Alzheimer's disease. Yet to be determined is the significance of how smoking tobacco influences the nicotinic receptor function and etiology of Alzheimer's disease. There has been an indication that nicotine receptor function may be abnormal in Alzheimer's disease and this dysfunction may be due to the loss of an endogenous compound which inhibits normal nicotine binding.3 An alternative suggestion from our results is that susceptibility to smoking and a protective mechanism against Alzheimer's disease are coinherited or coacquired.
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Grossberg et al. (1989) studied this question.
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