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Investigates sleep measures and amyloid deposition in the aging population, suggesting early intervention potential.
INTRODUCTION Poor sleep is a symptom and candidate risk factor for Alzheimer's disease (AD). We investigated whether objective and subjective longitudinal sleep measures correlated with AD pathology at brain autopsy. METHODS Rush Memory and Aging Project (MAP) participants ( n = 798; Mean age at baseline = 81.72) underwent annual evaluation with actigraphy along with sleep questionnaires and cognitive assessment. Brain autopsy provided quantitative neuropathologic data. RESULTS Objective sleep fragmentation was associated with higher amyloid density. This association was only observed among individuals with low AD neuropathologic change or no/mild cognitive impairment. Last‐measured sleep fragmentation had a stronger association with amyloid density than did mean sleep fragmentation across the study. Poorer subjective sleep quality was paradoxically linked to lower AD‐related neuropathologic burden. DISCUSSION These findings provide histopathologic evidence linking objectively measured sleep fragmentation to cerebral amyloid deposition and suggest that sleep disruption may be most relevant during earlier stages of AD pathogenesis.
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Rudolf et al. (2026) studied this question.
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