Deciphering and Restoring Computational Setpoints in Alzheimer’s Disease Through Sleep-Enhanced Network Homeostasis


Alzheimer’s disease, a debilitating form of dementia, profoundly impairs the brain’s ability to process complex information, gradually eroding memory, understanding and physical control. Despite knowing that the buildup of abnormal proteins like tau and amyloid beta contribute to the disease, the specific breakdowns in how brain cells communicate—and the resulting loss of brain function—are not fully understood. Our research proposes a novel perspective: to explore how Alzheimer’s disease disrupts the “mathematical rules” that govern healthy brain activity. Our preliminary data suggests that while individual neurons—the brain’s signaling cells—remain surprisingly resilient, the broader network, which integrates information across the brain, fails. This network collapse notably parallels the deterioration of sleep patterns, one of the earliest signs of Alzheimer’s. Sleep is crucial, as it appears to recalibrate the brain’s information-processing abilities. Our study seeks to determine whether the decline in the brain’s self-restoration through sleep is an early trigger of Alzheimer’s. Moreover, by enhancing sleep before Alzheimer’s disease fully develops, we plan to test whether we can strengthen the brain’s processing abilities, and thereby slow down or even prevent disease progression. This approach shifts the focus from simply trying to limit cell damage to actively reinforcing the brain’s own mechanisms for preserving its function. We aim to uncover the underpinnings of both brain resilience and vulnerability to Alzheimer’s disease, paving the way for groundbreaking strategies that can restore brain health and halt disease advancement.

Funding to Date



Studies of Alternative Neurodegenerative Pathways, Translational


Keith Hengen, Ph.D.