Impaired sleep is associated with a higher rate of future β-amyloid accumulation.
Slow-wave activity and sleep efficiency both forecast this increase in β-amyloid.
Sleep may serve as a marker of future Alzheimer’s disease risk and the speed of progression.
Experimental sleep-wake disruption in rodents and humans causally modulates β-amyloid (Aβ) dynamics (e.g., [ 1 , 2 , 3 ]). This leads to the hypothesis that, beyond cross-sectional associations, impaired sleep structure and physiology could represent prospective biomarkers of the speed with which Aβ accumulates over time. Here, we test the hypothesis that initial baseline measures of non-rapid eye movement (NREM) sleep slow-wave activity (SWA) and sleep quality (efficiency) provide future forecasting sensitivity to the rate of Aβ accumulation over subsequent years. A cohort of clinically normal older adults was assessed using objective sleep polysomnography in combination with longitudinal tracking of Aβ accumulation with [ 11C]PiB positron emission tomography (PET) imaging…