Key Project Outcomes
Reliable prognostic biomarkers for Alzheimer disease (AD) remain elusive. Given that sleep and cognition share biological regulatory mechanisms, this project was designed to characterize the association between sleep disturbances and novel imaging markers of AD in relation to cognitive decline.
Results are still preliminary, but we found relationships between time spent in deep slow-wave sleep and REM sleep with PET tracers labeling the hallmark pathologies of AD ,tau, at early stages. Another hallmark tracer, amyloid beta, was associated with poor sleep efficiency.
In addition, poor cognitive performance based on the Preclinical Alzheimer’s Cognitive Composite was associated with lack of deeper sleep stages and sleep efficiency.
Additional analysis looking further at the sleep microstructure are still ongoing.
So far our results suggest that age-dependent cognitive changes may be related to changes in sleep, and sleep disruption may drive or reflect the accumulation of the two hallmark imaging markers of AD, amyloid beta and tau.
Sleep disturbances thereby have a potential to serve as surrogate markers for cognitive decline, help predict individuals at risk for AD and potentially offer new approaches for therapeutic targets.
Linking Sleep Disturbances with Amyloid and Tau Imaging. Preliminary Findings from the Harvard Aging Brain Study
APOE-ε4 is associated with impaired sleep-dependent memory consolidation in healthy carriers