Abstract
AbstractBackgroundAmyloid‐β is a classical hallmark and risk factor for development of Alzheimer’s disease (AD). Observational data suggest that having higher body mass index (BMI) is associated with lower cerebral amyloid burden in cognitively normal adults. However, the influence of body composition on cerebral amyloid deposition has not been investigated. We investigated whether baseline body composition influences 1‐year change in cerebral amyloid in a sample enriched with older adults with elevated amyloid.MethodData from 103 cognitively normal adults with high normal or elevated cerebral amyloid that participated in a 1‐year exercise RCT were analyzed. Cerebral amyloid burden was quantified in 6 cortical regions of interest by Florbetapir F18 PET. Global amyloid burden was calculated by averaging the 6 regions. Total lean body mass and fat mass percentages were measured using DXA. We constructed ordinary least squares regression models to investigate the relationship between our baseline measures of body composition and 1‐year change in regional and global amyloid. All models included age, APOE4 carrier status, study arm, sex, and baseline regional amyloid standard uptake value ratios as covariates.ResultParticipants were 67% female with a mean age of 72.4 ± 5.0 years. Mean BMI was 28.0 ± 5.4, lean body mass percentage was 61% ± 7.5%, and fat mass percentage was 38% ± 7.1%. Higher BMI was related to less 1‐year amyloid accumulation in 5 regions (anterior cingulate gyrus, precuneus, inferior medial frontal gyrus, lateral temporal lobe, and superior parietal lobe) and globally (β range = ‐0.003 to ‐0.004, p<0.03 for all). Higher fat mass percentage was related to less amyloid accumulation in all 6 brain regions and the global average (β range = ‐0.25 to ‐0.34, p<0.03 for all). Higher lean body mass percentage was related to less amyloid accumulation in the lateral temporal lobe (β = ‐0.003, p = 0.01).ConclusionIn this study, having larger body stature and higher fat mass percentage were related to less amyloid accumulation in individuals with elevated risk for AD. Further studies are necessary to explore these relationships in greater detail and to ascertain if these findings are modulated by other biological variables.
Published Version
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