Night-to-night REM sleep variability emerges as an early marker for cerebral amyloid-β deposition.

Alzheimer's disease (AD) is characterized by progressive neurodegeneration, with amyloid-β (Aβ) plaque accumulation being a hallmark pathology that often precedes clinical symptoms by decades. Sleep disturbances, particularly alterations in rapid eye movement (REM) sleep), are increasingly recognized as early indicators and potential contributors to AD pathogenesis. Current diagnostic methods for early AD, such as PET imaging for Aβ, are costly and not widely accessible, highlighting a critical need for non-invasive, scalable biomarkers. Understanding the relationship between sleep architecture and early Aβ deposition could offer novel avenues for risk stratification and intervention.

Researchers investigated sleep alterations in a cohort of cognitively unimpaired older adults to assess associations with regional amyloid-β deposition. Participants underwent comprehensive sleep monitoring, likely via polysomnography (PSG), to quantify night-to-night variability in REM sleep parameters. Cerebral amyloid-β burden was simultaneously assessed using positron emission tomography (PET) imaging with specific tracers to quantify Aβ accumulation. The study aimed to identify if specific sleep architecture changes, particularly in REM sleep, correlated with early Aβ pathology.