Alzheimer's disease is widely recognized for memory loss, but sleep disruption is one of its earliest warning signs, appearing years before cognitive decline becomes apparent. People with Alzheimer's experience fragmented sleep and a loss of the deep, slow-wave sleep that the brain depends on for restoration. Importantly, deep sleep actively drives cerebrospinal fluid (CSF) flow through the brain, powering a clearance system called the glymphatic network that flushes out toxic proteins, including amyloid and tau, the molecular hallmarks of Alzheimer's pathology. Aging impairs this clearance system, and we suspect that sleep disruption in Alzheimer's makes it worse. However, the causal relationship has never been directly tested, and no one has shown whether restoring CSF flow can improve sleep in a diseased brain. Our team is addressing this with a noninvasive ultrasound approach called ultrasonic debris clearance (UDC), developed in the Airan lab at Stanford, that enhances CSF flow without surgery or drugs. Working across four complementary laboratories, we are measuring sleep patterns, CSF flow dynamics, and CSF molecular composition in a mouse model of Alzheimer's disease, before and after UDC treatment. The Fame lab contributes high-sensitivity protein profiling of CSF; the Gibson lab brings expertise in how neurodegeneration disrupts sleep and glial biology; the Giardino lab provides sleep monitoring and quantitative behavioral analysis. Together, we are testing whether enhancing brain clearance can restore healthy sleep and normalize disease-related proteins in the CSF, opening a tractable avenue for early intervention in Alzheimer's disease.