Journal
NEUROLOGY
Volume 75, Issue 22, Pages 1982-1987Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181ffe4f6
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Funding
- Alzheimer's Association [IIRG-06-27261]
- Internationale Stichting Alzheimer Onderzoek
- Erasmus MC University Medical Center and Erasmus University Rotterdam
- Netherlands Organization for Scientific Research
- Netherlands Organization for Health Research and Development
- Research Institute for Diseases in the Elderly
- Ministry of Education, Culture and Science
- Ministry of Health, Welfare and Sports
- European Commission
- Municipality of Rotterdam
- Netherlands Consortium for Healthy Ageing
- Netherlands Heart Foundation
- Pfizer Inc,
- Merck Sharp Dohme
- GlaxoSmithKline
- publication of Grondslagen der epidemiologie
- Klinische epidemiologie
- Investigating Neurological Disease (Cambridge University)
- Netherlands Genomics Initiative for the Rotterdam Study
- Ministry of Health for the Generation R study
- publication of Neurologie
- Anamnese en lichamelijk onderzoek
- Neurovascular Research Fund Rotterdam
- Alzheimer's Association USA
- NIH [1 R01 AG 033 193-01]
- Internationale Stichting Alzheimer Onderzoek (ISAO)
- Dutch Cancer Society
- Dutch Parkinsonfonds
- Netherlands Brain Foundation
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Objective: Diabetes mellitus has been associated with an increased risk of Alzheimer disease (AD), but how it exerts its effect remains controversial. Possible pathophysiologic mechanisms are glucose toxicity and a direct effect of insulin on amyloid metabolism. Most studies had short follow-up, and longer-term effects of diabetes on AD risk are unknown. We investigated whether fasting glucose and insulin levels and insulin resistance are associated with the risk of AD and whether this risk is constant over time. Methods: The study was based on 3,139 participants of the Rotterdam Study, a population-based cohort study. All subjects were free from dementia, did not have a history of diabetes, and had fasting levels of glucose and insulin measured at baseline. Insulin resistance was estimated with the homeostasis model assessment. We investigated how fasting glucose, insulin, and insulin resistance are related to the risk of AD in 3 different strata according to time-to-event, using Cox proportional hazards models. Results: During follow-up, 211 participants developed AD, 71 of them within 3 years of baseline. Levels of insulin and insulin resistance were associated with a higher risk of AD within 3 years of baseline. After 3 years, the risk was no longer increased. Glucose was not associated with a higher risk of AD. There was no interaction of APOE epsilon 4 carriership and insulin metabolism on the risk of AD. Conclusions: Our findings suggest that insulin metabolism influences the clinical manifestation of AD only within 3 years. Neurology (R) 2010;75:1982-1987
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