期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 69, 期 3, 页码 817-827出版社
IOS PRESS
DOI: 10.3233/JAD-190154
关键词
Alzheimer disease; amyloid-beta; apolipoproteins E; body mass index; obesity; positron emission tomography
资金
- BrightFocus Foundation [A2017272S, A2017330S]
- Alzheimer's Association Research Grant [AARG-17-532945]
- Arizona Alzheimer's Research Consortium
- NIH/NIA [R01AG055444, R01AG031581]
- Longer Life Foundation
- NIH [P50AG005681, P01AG026276, P01AG003991, UL1TR000448, 1P30NS098577, R01 EB009352]
- Non-NIH: The Charles and Joanne Knight Alzheimer Disease Research Center Support Fund
- David and Betty Farrell Medical Research Fund
- Daniel J Brennan Alzheimer Research Fund
- Thomas E. Brew Foundation Fund
- Fred Simmons and Olga Mohan Alzheimer Research Support Fund
- BarnesJewish Hospital Foundation (BJHF)
- Willman Scholar Fund (BJHF)
- Avid Radiopharmaceuticals
Background: Both low and high body mass index (BMI) have been associated with an increased risk of dementia, including that caused by Alzheimer's disease (AD). Specifically, high middle-age BMI or a low late-age BMI has been considered a predictor for the development of AD dementia. Less studied is the relationship between BMI and AD pathology. Objective: We explored the association between BMI and cortical amyloid-beta (A beta) burden in cognitively normal participants that were either in mid-life (45-60 years) or late-life (>60). Methods: We analyzed cross-sectional baseline data from the Knight Alzheimer Disease Research Center (ADRC) at Washington University. A beta pathology was measured in 373 individuals with A beta PET imaging and was quantified using Centiloid units. We split the cohort into mid- and late-life groups for analyses (n = 96 and n = 277, respectively). We ran general linear regression models to predict A beta levels from BMI while controlling for age, sex, years of education, and APOE4 status. Analyses were also conducted to test the interaction between BMI and APOE4 genotype and between BMI and sex. Results: Higher BMI was associated with lower cortical A beta burden in late-life (beta = -0.81, p = 0.0066), but no relationship was found in mid-life (beta = 0.04, p > 0.5). The BMI x APOE4+ and BMI x male interaction terms were not significant in the mid-life (beta = 0.28, p = 0.41; beta = 0.64, p = 0.13) or the late-life (beta= 0.17, p > 0.5; beta= 0.50, p = 0.43) groups. Conclusion: Higher late-life BMI is associated with lower cortical A beta burden in cognitively normal individuals.
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