My research investigates how disrupted circadian rhythms and sleep amplify neuroinflammation to drive Alzheimer's disease (AD) progression, with the goal of identifying mechanisms and therapeutic targets that operate upstream of classical amyloid and tau pathology.

Circadian disruptions — from shift work, irregular sleep, and nighttime light exposure — are increasingly recognized as modifiable AD risk factors, yet the underlying biology remains poorly understood. Using mouse models, my work shows that circadian misalignment activates inflammatory glial responses and disrupts fundamental cellular processes independent of amyloid precursor protein processing, pointing to a novel glial-mediated pathway through which lifestyle-driven circadian disruption may accelerate AD. In parallel, I have shown that FDA-approved orexin-targeting sleep medications promote a beneficial, phagocytic microglial phenotype and substantially reduce amyloid burden in mouse models.

More broadly, I am interested in identifying the full range of biological processes through which circadian and sleep disruption influence AD risk — and in translating those mechanisms into therapeutic targets. Together, these efforts position circadian health and sleep quality as tractable intervention points for AD prevention and treatment