Sleep Fragmentation and Sleep Stages 1 and 2 Are Associated With Amyloid‐Beta Burden in Cognitively Normal Older Adults

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Insomnia increases the risk of Alzheimer's disease and is associated with increased amyloid-β (Aβ) levels, but assessments using rigorous objective measures are lacking. The purpose of this cross-sectional study was to determine the association between sleep characteristics and Aβ burden using polysomnography and positron emission tomography (PET). Cognitively normal older adults (ages 60-85) with symptoms of insomnia underwent PET and overnight polysomnography. Pearson correlations determined the association between sleep variables and the standard uptake values ratio (SUVR) within global cerebral cortex, precuneus, posterior cingulate cortex (PCC), and the medial prefrontal cortex (mPFC). Multivariable stepwise regression was performed for each region of interest with apolipoprotein-ε (APOE) genotype and age as potential covariates. Sleep parameters between those who were Aβ elevated vs. non-elevated were compared using t-tests. Forty-three adults (69.3 ± 5.5 years old; 32.6% Aβ elevated; mostly non-Hispanic white and female) were included in analyses. Longer stage 1 was related to greater cortical and mPFC SUVR, greater wake after sleep onset was related to greater cortical, mPFC, and precuneus SUVR, and shorter stage 2 was associated with greater PCC SUVR. Compared to those who were Aβ non-elevated, those who were Aβ elevated had longer stage 1 and shorter stage 2 sleep. Greater sleep fragmentation, longer stage 1 sleep, and shorter stage 2 sleep were associated with greater Aβ burden in various regions of the brain in cognitively normal older adults. The results support poor sleep as an early risk factor for Aβ accumulation and possible target for Alzheimer's prevention. Trial Registration: The study was registered on clinicaltrials.gov (NCT03954210).

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