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Background: The purpose of this study was to examine if Type 2 diabetes mellitus is a risk factor for dementia in very old age, specifically for Alzheimer's disease (AD) and vascular dementia (VaD). Methods: We evaluated the risk of dementia in relation to Type 2 diabetes using a population-based sample of 702 individuals aged 80 years and older (mean age 83 years). A total of 187 persons received a dementia diagnosis. Thirty-one individuals had a diabetes diagnosis prior to onset of the dementia. Results: Cox proportional hazard analyses, adjusted for age, gender, education, smoking habits, and circulatory diseases, indicated an elevated risk to develop VaD (relative risk = 2.54, 95% confidence interval 1.35–4.78) in individuals with diabetes mellitus. No association was found between diabetes and AD. Conclusion: Type 2 diabetes is selectively related to the different subtypes of dementia. There is no increased risk of AD but more than a twofold risk of VaD in persons with diabetes.
We examined change in neuropsychological test performance related to
type 2 diabetes mellitus across a 6-year interval. A population-based
sample of 274 elderly participants (36 with diabetes and 238 without
diabetes) was examined at four occasions at a 2-year interval. The
participants were 80–93 years of age (M = 82.8 years)
and without dementia at baseline. The test battery included tests of
speed, visuospatial ability, short-term memory, semantic memory,
episodic memory, and the Mini Mental Status Examination. Several
models, taking into account diabetes and demographic data, were
analyzed using SAS Proc Mixed multilevel modeling. At baseline, there
were no significant differences in the neuropsychological tests related
to diabetes. The longitudinal analyses, however, showed that diabetes
was a significant predictor of decline for many of the tests. These
findings points to the conclusion that type 2 diabetes is associated
with accelerated cognitive decline in old age that may result in
dementia. (JINS, 2004, 10, 599–607.)
A method is presented for partitioning the variance associated with human smoking behavior into additive genetic, nonadditive genetic, prenatal environmental, postnatal familial environmental, and postnatal extrafamilial environmental components. Estimations can also be made of additive genetic and residual correlations between spouses and of the correlation between parental additive genetic effect and progeny nonadditive genetic and environmental effect. The variance estimates are free of the biases that might result from these correlations. The statistical genetic analysis is being applied to a large group of MZ and DZ twins, their spouses, and their adult children who live in southern Sweden. Blood samples from each subject will be used to identify their genetic constitution for a number of biochemical polymorphisms, some of which may be considered a priori to have possible relationships to smoking. Associations and genetic linkages between biochemical marker loci and quantitative behavioral traits will be sought. Traits of interest include a wide array of tobacco-use variables, motives for smoking, personality and cognitive variables, and other variables associated with drug use and health. Zygosity determinations based on biochemical polymorphisms have indicated MZ to DZ and DZ to MZ misclassification rates of 0% and 6.15%, respectively, when based solely on external morphology and questionnaire data. The nonpaternity ratio of the fathers with respect to their supposedly biological children is estimated to be 0.28%. Gene frequency estimates for 21 marker loci show that the sample of twins and their relatives is quite representative of the Swedish population at large. All loci were in Hardy-Weinberg-Castle equilibrium, with no evidence of assortative mating for biochemical traits. The MZ twins are significantly more concordant than the DZ twins with respect to whether they have ever had a smoking habit.
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