Abstract
BackgroundVery little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimer’s disease (AD) pathologies. This study aimed to examine the relationship between sleep experiences during the young adulthood, midlife, and late-life periods and in vivo cerebral beta-amyloid (Aβ) deposition and AD signature regional neurodegeneration in cognitively normal (CN) old adults.MethodsThis study included 202 CN old adults who participated in the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE) study. All participants underwent a comprehensive clinical assessment, [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] Fluorodeoxyglucose-PET, and magnetic resonance imaging. The quality and duration of sleep were assessed for the following age periods: 20–30s, 40–50s, and the most recent month. All analyses were adjusted for age, gender, education, apolipoprotein E ε4 status, vascular risk score, Hamilton Depression Rating Scale score, and use of sleep medication.ResultsBad sleep quality and short sleep duration during midlife were significantly associated with increased Aβ deposition and AD signature regional hypometabolism, respectively. Although current bad sleep quality appeared to be associated with increased Aβ accumulation, this association disappeared after controlling for the effects of midlife sleep quality. Neither the quality nor duration of sleep during young adulthood was related to Aβ burden or neurodegeneration.ConclusionsBad sleep quality during midlife increases pathological Aβ deposition in the brain, while short sleep duration during the same period accelerates regional hypometabolism.
Highlights
Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimer’s disease (AD) pathologies
Several clinical studies based on amyloid positron emission tomography (PET) imaging have revealed that poorer self-reported sleep quality is associated with a greater in vivo Aβ burden in the human brain [8,9,10,11], while the association between self-reported sleep duration and Aβ deposition is controversial [8, 10,11,12]
Current bad sleep quality appeared to be associated with increased Aβ accumulation, this relationship disappeared after controlling for the effects of midlife sleep quality
Summary
Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimer’s disease (AD) pathologies. Two translational human studies partly demonstrated the causal relationship; Choe et al Alzheimer's Research & Therapy (2019) 11:79 one night of sleep deprivation increased cerebrospinal fluid (CSF) Aβ42 [13], and slow-wave activity disruption increased CSF Aβ40 [14]. They only tested the acute effect of disrupted sleep, which may differ from the lifelong effects of poor sleep
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
