My research program is composed of understanding the role of circadian function on memory during aging and Alzheimer’s disease (AD) progression. A growing body of evidence suggests that disruptions to the circadian system occur prior to the clinical onset of memory deficits in AD. Therefore, circadian function may be a modifiable risk factor for AD. We recently reported that the circadian system influences amyloid-β dynamics and pathology in a mouse model of AD (Kress et al., 2018 JEM). In my laboratory, we are extending this work to look in detail at how the circadian system may influence AD pathogenesis. This program has the potential to provide important advances to our basic understanding for the role of circadian function on memory. Moreover, it provides important information to identify pathophysiology changes, mechanisms, and possible strategies to ameliorate AD progression. Because sleep-wake and circadian disruption are major causes of morbidity and institutionalization among AD patients, we hope that these studies may lead to effective interventions to promote healthy aging and forestall disease progression, which would benefit the individual as well as lessen caregiver burden and decrease financial care costs associated with progressing dementia.