Neuroimaging biomarkers of the Amyloid, Tau, Neurodegeneration and Vascular framework in association with sleep duration changes over time

Background Both short and long sleep duration were previously associated with incident dementia, but underlying mechanisms of this association remains unknown. This project aims to evaluate how self-reported its change over time associate (A)myloid, (T)au, (N)eurodegeneration (V)ascular neuroimaging markers Alzheimer’s disease (AD). Method Within the Framingham Heart Study, two samples studied: 271 participants (age:53.6±8.0 years; 51%M) who underwent 11C-PiB amyloid (global, precuneus) 18F-Flortaucipir tau (several medial cortical limbic structures) PET imaging; 2165 (age:61.3±11.1 45%M) an MRI. To estimate neurodegeneration, total brain volume was extracted from Vascular MRI metrics included white matter hyperintensities (continuous, dichotomous indicator for extensive age), covert infarcts, average free-water. Self-reported assessed both at testing around 15 years before, split by categories (≤6h, 7-8h, ≥9h). Sleep between continuous delta (split negative positive values decreased or increased respectively). Logistic linear regression models tested metrics, adjusted age age2, sex, camera, APOE4 carrier status, depression, diabetes, hypertension, prevalent cardiovascular diseases. Results No observed cross-sectional metrics. Transitioning longer (≤6h ≥9h 7-8h as compared consistently sleeping 7-8h) higher burden (extensive, OR[95%CI]:3.50[0.95-12.92], p = 0.040;ß[SE]:0.25[0.10], 0.015) free-water (ß[SE]:0.021[0.007], 0.003;ß[SE]:0.009[0.002], 0.0002). When looking change, increasing also OR[95%CI]:1.26[1.02-1.55], 0.032;ß[SE]:0.10[0.04], 0.007) (ß[SE]:0.002[0.001], 0.031). not outcomes. Conclusion pathology in evidenced is that getting time, thus potentially explaining dementia risk. In fact, elongation may be early AD trajectory.