Abstract
Alzheimer’s disease (AD) is characterized by a progressive loss of memory and cognition, for which there is no cure. Human genetics supports a primary role for β-amyloid in AD and many other genetic factors contributing to the risk of AD have been identified, but the options for treatment remain limited. We examine disruptions at the neural circuit level and determine its role in the etiology of AD. We recently discovered that using sensory stimuli to entrain neural oscillations at gamma frequencies leads to a reduction of amyloid and Tau pathology in AD mouse models. I will discuss the potential mechanisms by which sensory gamma entrainment elicits it’s neuroprotective effects.