期刊
NEUROLOGY
卷 75, 期 9, 页码 764-770出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181eee25f
关键词
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资金
- Ministry of Health, Labour and Welfare, Japan [H19-nanchi-ippan-006]
- Ministry of Health, Labour and Welfare [H20-Chouju-004]
- Ministry of Education, Culture, Sports, Science and Technology of Japan [19300125]
- Eli Lilly Co.
- GlaxoSmithKline
- Pfizer Inc.
- Asahi Kasei Corporation
- Janssen
- Tsumura Co.
- Ajinomoto Co., Inc.
- Mitsubishi Tanabe Pharma Corporation
- Meiji Techno Co. Ltd.
- Kyowa Hakko Kirin Pharma, Inc.
- Dainippon Sumitomo Pharma Co., Ltd.
- Organon International (Schering-Plough Corp.)
- Otsuka Pharmaceutical Co., Ltd.
- Grants-in-Aid for Scientific Research [19300125] Funding Source: KAKEN
Objective: We examined the association between diabetes-related factors and pathology of Alzheimer disease (AD) to evaluate how diabetes affects the pathogenic process of AD. Methods: This study included specimens from a series of 135 autopsies of residents of the town of Hisayama in Fukuoka prefecture (74 men and 61 women) performed between 1998 and 2003, who underwent a 75-g oral glucose tolerance test in clinical examinations in 1988. We measured diabetes-related factors including fasting glucose, 2-hour post-load plasma glucose, fasting insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) in 1988. Neuritic plaques (NPs) were assessed according to the Consortium to Establish a Registry for Alzheimer's Disease guidelines and neurofibrillary tangles (NFTs) were assessed according to Braak stage. The associations between each factor and AD pathology were examined by analysis of covariance and logistic regression analyses. Results: Higher levels of 2-hour post-load plasma glucose, fasting insulin, and HOMA-IR were associated with increased risk for NPs after adjustment for age, sex, systolic blood pressure, total cholesterol, body mass index, habitual smoking, regular exercise, and cerebrovascular disease. However, there were no relationships between diabetes-related factors and NFTs. Regarding the effects of APOE genotype on the risk of AD pathology, the coexistence of hyperglycemia and APOE epsilon 4 increased the risk for NP formation. A similar enhancement was observed for hyperinsulinemia and high HOMA-IR. Conclusion: The results of this study suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate NP formation in combination with the effects of APOE epsilon 4. Neurology (R) 2010;75:764-770
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