Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
Sleep fragmentation correlates with amyloid beta deposition at brain autopsy.
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Rudolf Mark A, Ng Yee To, Lieberman Andrew P
Аннотация
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; Meanage 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.
METHODS: Rush Memory and Aging Project (MAP) participants (n = 798; Meanage 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.