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Midlife insulin resistance, APOE genotype, and late-life brain amyloid accumulation
Umeå University, Faculty of Medicine, Department of Radiation Sciences. Turku PET Centre, University of Turku, Finland.
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2018 (English)In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 90, no 13, p. e1150-e1157Article in journal (Refereed) Published
Abstract [en]

Objective To examine whether midlife insulin resistance is an independent risk factor for brain amyloid accumulation in vivo after 15 years, and whether this risk is modulated by APOE epsilon 4 genotype. Methods This observational study examined 60 elderly volunteers without dementia (mean age at baseline 55.4 and at follow-up 70.9 years, 55.5% women) from the Finnish population-based, nationwide Health2000 study with [C-11]Pittsburgh compound B-PET imaging in 2014-2016. The participants were recruited according to their homeostatic model assessment of insulin resistance (HOMA-IR) values in the year 2000, and their APOE epsilon 4 genotype. The exposure group (IR+, n = 30) consisted of individuals with HOMA-IR > 2.17 at baseline (highest tertile of the Health2000 study population), and the control group (IR-, n = 30) consisted of individuals with HOMA-IR < 1.25 at baseline (lowest tertile). The groups were enriched for APOE epsilon 4 carriers, resulting in 50% (n = 15) APOE epsilon 4 carriers in both groups. Analyses were performed with multivariate logistic and linear regression. Results An amyloid-positive PET scan was found in 33.3% of the IR-group and 60.0% of the IR+ group (odds ratio 3.0, 95% confidence interval 1.1-8.9, p = 0.04). The increased risk was seen in carriers and noncarriers of APOE epsilon 4 genotype. Higher midlife, but not late-life continuous HOMA-IR was associated with a greater brain amyloid burden at follow-up after multivariate adjustments for other cognitive and metabolic risk factors (ss = 0.11, 95% confidence interval 0.002-0.22, p = 0.04). Conclusions These results indicate that midlife insulin resistance is an independent risk factor for brain amyloid accumulation in elderly individuals without dementia.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2018. Vol. 90, no 13, p. e1150-e1157
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Neurology Neurosciences
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URN: urn:nbn:se:umu:diva-150496DOI: 10.1212/WNL.0000000000005214ISI: 000439102000008PubMedID: 29476033OAI: oai:DiVA.org:umu-150496DiVA, id: diva2:1238310
Available from: 2018-08-13 Created: 2018-08-13 Last updated: 2018-08-13Bibliographically approved

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