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From the John A. Burns School of Medicine (Drs. Curb, Rodriguez, Petrovitch, Masaki, and Blanchette), University of Hawaii at Manoa; Honolulu Heart Program (Drs. Curb, Rodriguez, Abbott, Petrovitch, Ross, Masaki, and White, and R. Chen), Kuakini Medical Center, Honolulu; University of Virginia (Dr. Abbott), Charlottesville, VA; the National Institute on Aging (D. Foley, and Drs. Harris and White), Bethesda, MD, and Honolulu; and the Department of Veterans Affairs (Dr. Ross), Honolulu, HI.
Address correspondence and reprint requests to Dr. J. David Curb, John A. Burns School of Medicine, Division of Geriatric Medicine, University of Hawaii, 347 N. Kuakini Street, Honolulu, HI 96817.
OBJECTIVE: To assess the relationship between impaired glucose tolerance and both vascular dementia and AD.
BACKGROUND: Diabetes and abnormalities of glucose metabolism have been associated with stroke and poor cognitive function. In addition, glycoproteins and glycosylation have been postulated to be associated with the development of neuritic plaques characteristic of AD.
METHODS: A historical prospective cohort study of Japanese-American men (n = 3,774), who were examined at ages 45 to 68 (1965 through 1968) and again at ages 71 to 93 (1991 through 1993). Measurements were obtained by clinical and home examinations: assessment of glucose intolerance (nonfasting 1 hour after glucose load) from 1965 through 1968 and history of diabetes diagnosed by a physician at examinations given from 1965 through 1968 and from 1976 through 1978. At the 1991 through 1993 examinations, the Cognitive Assessment Screening Instrument (CASI)an instrument designed for use in cross-cultural settings combining features of the Folstein Mini-Mental State Examination, the Modified Mini-Mental State Examination, and the Hasegawa Dementia Screening Scalewas used. Diagnosis and classification of AD and vascular dementia were made by a consensus panel using neuropsychologic assessment data, a neurologists evaluation, and information from a family informant. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed., revised criteria were used to establish dementia, and subclassification by cause was based on other published criteria.
RESULTS: No association between AD and diabetes, present either 25 or 15 years previously, was found after adjustment for age and education in a multiple regression model. A significant association was found between impaired glucose tolerance at baseline and vascular dementia (p < 0.01).
CONCLUSIONS: These findings confirm expected relationships between impaired glucose tolerance and stroke-related dementia but do not support an association of disordered glucose metabolism with AD.
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