Higher Body Mass Index Is Associated with Lower Cortical Amyloid-β Burden in Cognitively Normal Individuals in Late-Life.

Abstract

BACKGROUND\nBoth 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.\n\n\nOBJECTIVE\nWe explored the association between BMI and cortical amyloid-β (Aβ) burden in cognitively normal participants that were either in mid-life (45-60 years) or late-life (>60).\n\n\nMETHODS\nWe analyzed cross-sectional baseline data from the Knight Alzheimer Disease Research Center (ADRC) at Washington University. Aβ pathology was measured in 373 individuals with Aβ PET imaging and was quantified using Centiloid units. We split the cohort into mid- and late-life groups for analyses (n\u200a=\u200a96 and n\u200a=\u200a277, respectively). We ran general linear regression models to predict Aβ 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.\n\n\nRESULTS\nHigher BMI was associated with lower cortical Aβ burden in late-life (β=\u200a-0.81, p\u200a=\u200a0.0066), but no relationship was found in mid-life (β=\u200a0.04, p\u200a>\u200a0.5). The BMI×APOE4+ and BMI×male interaction terms were not significant in the mid-life (β=\u200a0.28, p\u200a=\u200a0.41; β=\u200a0.64, p\u200a=\u200a0.13) or the late-life (β=\u200a0.17, p\u200a>\u200a0.5; β=\u200a0.50, p\u200a=\u200a0.43) groups.\n\n\nCONCLUSION\nHigher late-life BMI is associated with lower cortical Aβ burden in cognitively normal individuals.