The accelerating pace of research on sleep or circadian function and Alzheimer disease (AD) has raised the possibility of targeting sleep or circadian behaviors to mitigate AD risk. Sleep and circadian functions are separate but intertwined, in that circadian mechanisms coordinate physiological functions to the 24-hour clock for optimal function, including sleep-wake state. Accumulating data support a bidirectional association between AD pathology and sleep and circadian function. Even during the more than 15-year preclinical (presymptomatic) stage of AD, decreased sleep quality and fragmented circadian rhythms are associated with AD pathology.1,2 Conversely, sleep and circadian dysfunction, particularly slow-wave sleep disruption, elevates levels of amyloid-β and tau.3-5 Large longitudinal studies show that obstructive sleep apnea (OSA) and insufficient sleep increase risk of cognitive impairment.6,7 Given the high prevalence of sleep and circadian dysfunction, with an estimated 1 billion individuals worldwide having OSA, and 40% in a large survey conducted in the UK reporting insufficient sleep,7 sleep and circadian function may be a high-value target for intervention as a modifiable AD risk factor.