Sleep as a Window into Early Stages of Alzheimer's Pathophysiology: Implications for Clinical Development

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 analyses and go/no-go decisions. Speakers will address how biomarker-positive but cognitively normal patients can be identified through sleep EEG and enrolled earlier than current diagnostic pathways allow.
Attendees will learn how sleep EEG endpoints can be incorporated into trial design to help capture treatment signals earlier, support interim analyses, and characterize response.
Register for this webinar to learn how sleep EEG can support earlier detection of Alzheimer's pathophysiology and strengthen AD/MCI clinical trial design.

Who Should Attend
This webinar will appeal to:
Chief Medical Officers overseeing AD assets
Chief Scientific Officers overseeing AD assets
Clinical Development professionals working in the neurodegeneration space
Therapeutic Area Leads in Neurodegeneration or Neurology
Digital Health, Data Science and Biomarker Strategy professionals supporting trial innovation
CRO leaders and Decentralized Trial Specialists designing or executing remote study models
Neuroscience Business Unit Heads
US and Global Commercial Teams in Neuroscience
Chief Commercial Officers
Neurodegeneration Asset Leads

What You Will Learn
Attendees will gain insight into:
The mechanistic relationship between sleep disruption, slow-wave sleep and Alzheimer’s Pathophysiology
How sleep EEG can detect early biological changes in pre-clinical and MCI populations
Why sleep spindles, slow waves and sleep microarchitecture may support patient stratification and disease monitoring
How at-home EEG may help capture objective sleep endpoints at scale in AD/MCI trials
How sleep-based biomarkers can inform interim analyses, responder differentiation and go/no-go decisions

Register free on Xtalks:
https://xtalks.com/webinars/sleep-as-a-window-into-early-stages-of-alzheimers-pathophysiology-implications-for-clinical-development/