Sleep is fundamental to memory consolidation and neural repair, making it one of the most biologically meaningful signals we can measure in aging and neurodegeneration. Sleep disturbances are often among the earliest detectable changes in Alzheimer’s disease (AD), emerging years before memory loss, cognitive decline, and diagnosis, and potentially ahead of pathology accumulation itself. This webinar explores how sleep EEG can support earlier detection of Alzheimer’s pathophysiology and inform AD/Mild Cognitive Impairment (MCI) trial design. The featured speakers will examine how disrupted sleep is tied to pathways implicated in neurodegeneration, including synaptic homeostasis, neuroinflammation, metabolic waste clearance, and glial cell function, with slow-wave sleep thought to be central to the glymphatic clearance of amyloid-beta and tau. Poor sleep may accelerate pathological protein accumulation, which in turn degrades the brain regions that regulate sleep, making disrupted sleep both an early symptom and likely contributor to AD: disrupting slow-wave activity for a single night raises CSF amyloid-beta by morning, and reduced slow-wave activity separately tracks with greater amyloid burden on PET. The discussion will also address how sleep can serve both an early functional readout, ahead of standard cognitive testing, and a sensitive measure of clinical benefit. Spindle-slow wave coupling tracks early amyloid burden and predicts memory decline in cognitively healthy older adults, and because sleep metrics shift within days to months rather than the years needed for structural or cognitive endpoints, they can track amyloid accumulation and predict memory decline over 6- to 24-month windows, a timescale well suited to interim