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- Hassing, Linda, 1967, et al.
(author)
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Overweight in midlife and risk of dementia: a 40-year follow-up study
- 2009
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In: International Journal of Obesity. - : Springer. ; 33:8, s. 893-898
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Journal article (peer-reviewed)abstract
- Objective: This study examines whether overweight in midlife increases dementia risk later in life. Methods: In 1963 body mass index was assessed in 1152 participants of The Swedish Twin Registry, at the age of 45–65 years. These participants were later screened for dementia in a prospective study with up to 40 years follow-up. A total of 312 participants were diagnosed with dementia. Results: Logistic regression analyses adjusted for demographic factors, smoking and alcohol habits, indicated that men and women categorized as overweight in their midlife had an elevated risk of dementia (OR=1.59; 95% CI: 1.21–2.07, P=0.002), Alzheimer's disease (OR=1.71; 95% CI: 1.24–2.35, P=0.003), and vascular dementia (OR=1.55; 95% CI: 0.98–2.47, P=0.059). Further adjustments for diabetes and vascular diseases did not substantially affect the associations, except for vascular dementia (OR=1.36; 95% CI: 0.82–2.56, P=0.116), reflecting the significance of diabetes and vascular diseases in the etiology of vascular dementia. There was no significant interaction between overweight and APOE alt epsilon4 status, indicating that having both risk factors does not have a multiplicative effect with regard to dementia risk. Conclusions: This study gives further support to the notion that overweight in midlife increases later risk of dementia. The risk is increased for both Alzheimer's disease and vascular dementia, and follows the same pattern for men and women. Keywords: BMI, alzheimer's disease, vascular dementia, dementia, overweight, obesity
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- Reynolds, Chandra A, et al.
(author)
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A survey of ABCA1 sequence variation confirms association with dementia.
- 2009
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In: Human mutation. - : Hindawi Limited. - 1098-1004 .- 1059-7794. ; 30:9, s. 1348-54
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Journal article (peer-reviewed)abstract
- We and others have conducted targeted genetic association analyses of ABCA1 in relation to Alzheimer disease risk with a resultant mixture of both support and refutation, but all previous studies have been based upon only a few markers. Here, a detailed survey of genetic variation in the ABCA1 region has been performed in a total of 1,567 Swedish dementia cases (including 1,275 with Alzheimer disease) and 2,203 controls, providing evidence of association with maximum significance at marker rs2230805 (odds ratio [OR]=1.39; 95% confidence interval [CI] 1.23-1.57, p=7.7x10(-8)). Haplotype-based tests confirmed association of this genomic region after excluding rs2230805, and imputation did not reveal additional markers with greater support. Significantly associating markers reside in two distinct linkage disequilibrium blocks with maxima near the promoter and in the terminal exon of a truncated ABCA1 splice form. The putative risk allele of rs2230805 was also found to be associated with reduced cerebrospinal fluid levels of beta-amyloid. The strongest evidence of association was obtained when all forms of dementia were considered together, but effect sizes were similar when only confirmed Alzheimer disease cases were assessed. Results further implicate ABCA1 in dementia, reinforcing the putative involvement of lipid transport in neurodegenerative disease.
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