Abstract
BackgroundIn view of reported associations between high adiposity, particularly in midlife and late-life dementia risk, we aimed to determine associations between body mass index (BMI), and BMI changes across adulthood and brain structure and pathology at age 69–71 years.MethodsFour hundred sixty-five dementia-free participants from Insight 46, a sub-study of the British 1946 birth cohort, who had cross-sectional T1/FLAIR volumetric MRI, and florbetapir amyloid-PET imaging at age 69–71 years, were included in analyses. We quantified white matter hyperintensity volume (WMHV) using T1 and FLAIR 3D-MRI; β-amyloid (Aβ) positivity/negativity using a SUVR approach; and whole brain (WBV) and hippocampal volumes (HV) using 3D T1-MRI. We investigated the influence of BMI, and BMI changes at and between 36, 43, 53, 60–64, 69 and 71 years, on late-life WMHV, Aβ-status, WBV and mean HV. Analyses were repeated using overweight and obese status.ResultsAt no time-point was BMI, change in BMI or overweight/obese status associated with WMHV or WBV at age 69–71 years. Decreasing BMI in the 1–2 years before imaging was associated with an increased odds of being β-amyloid positive (OR 1.45, 95% confidence interval 1.09, 1.92). There were associations between being overweight and larger mean HV at ages 60–64 (β = 0.073 ml, 95% CI 0.009, 0.137), 69 (β = 0.076 ml, 95% CI 0.012, 0.140) and 71 years (β = 0.101 ml, 95% CI 0.037, 0.165). A similar, albeit weaker, trend was seen with obese status.ConclusionsUsing WMHV, β-amyloid status and brain volumes as indicators of brain health, we do not find evidence to explain reported associations between midlife obesity and late-life dementia risk. Declining BMI in later life may reflect preclinical Alzheimer’s disease.
Highlights
In view of reported associations between high adiposity, in midlife and late-life dementia risk, we aimed to determine associations between body mass index (BMI), and BMI changes across adulthood and brain structure and pathology at age 69–71 years
Positive associations have been reported between obesity and all-cause dementia [1, 2], and with clinicallydiagnosed vascular [3, 4] and Alzheimer’s disease (AD) dementia [5,6,7] with more consistent findings relating to midlife, rather than late life, adiposity [8,9,10]
Associations may be driven by downstream consequences of obesity on other vascular risk factors, namely hypertension, insulin resistance, and dyslipidaemia [11], which have all been independently implicated in dementia risk
Summary
In view of reported associations between high adiposity, in midlife and late-life dementia risk, we aimed to determine associations between body mass index (BMI), and BMI changes across adulthood and brain structure and pathology at age 69–71 years. Vascular risk factors, including obesity, have been implicated as potential targets for intervention to reduce dementia risk. It remains unclear how obesity might influence subsequent brain health, and whether there are sensitive age periods when risk exposure is damaging. Positive associations have been reported between obesity and all-cause dementia [1, 2], and with clinicallydiagnosed vascular [3, 4] and Alzheimer’s disease (AD) dementia [5,6,7] with more consistent findings relating to midlife, rather than late life, adiposity [8,9,10]. Obesity influences cardiovascular health via endothelial dysfunction and proinflammatory routes [12], which might be implicated in cerebral health
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