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Sleep experiences during different lifetime periods and in vivo Alzheimer pathologies

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dc.contributor.authorChoe, Young Min-
dc.contributor.authorByun, Min Soo-
dc.contributor.authorYi, Dahyun-
dc.contributor.authorLee, Jun Ho-
dc.contributor.authorJeon, So Yeon-
dc.contributor.authorSohn, Bo Kyung-
dc.contributor.authorKim, Yu Kyeong-
dc.contributor.authorShin, Seong A-
dc.contributor.authorSohn, Chul-Ho-
dc.contributor.authorLee, Yu Jin-
dc.contributor.authorLee, Dong Young-
dc.date.accessioned2019-11-07T05:39:07Z-
dc.date.available2019-11-07T14:42:26Z-
dc.date.issued2019-09-12-
dc.identifier.citationAlzheimer's Research & Therapy, 11(1):79ko_KR
dc.identifier.issn1758-9193-
dc.identifier.urihttps://hdl.handle.net/10371/162643-
dc.description.abstractBackground
Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimers 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.

Methods
This study included 202 CN old adults who participated in the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimers 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.

Results
Bad 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.

Conclusions
Bad sleep quality during midlife increases pathological Aβ deposition in the brain, while short sleep duration during the same period accelerates regional hypometabolism.
ko_KR
dc.description.sponsorshipThis study was supported by a grant from the Ministry of Science, ICT, and Future Planning, Republic of Korea (Grant No: NRF-2014M3C7A1046042) and a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant No: HI18C0630). The funding source had no role in the design of the study; collection, analysis, and interpretation of the data; and writing of the manuscript.ko_KR
dc.language.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectMidlife sleepko_KR
dc.subjectPreclinical Alzheimer’s diseaseko_KR
dc.subjectCerebral amyloidko_KR
dc.subjectNeurodegenerationko_KR
dc.titleSleep experiences during different lifetime periods and in vivo Alzheimer pathologiesko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor최영민-
dc.contributor.AlternativeAuthor변민수-
dc.contributor.AlternativeAuthor이다현-
dc.contributor.AlternativeAuthor이준호-
dc.contributor.AlternativeAuthor전소연-
dc.contributor.AlternativeAuthor김유경-
dc.contributor.AlternativeAuthor신성아-
dc.contributor.AlternativeAuthor손철호-
dc.contributor.AlternativeAuthor이유진-
dc.contributor.AlternativeAuthor이동영-
dc.identifier.doi10.1186/s13195-019-0536-6-
dc.language.rfc3066en-
dc.rights.holderThe Author(s).-
dc.date.updated2019-09-15T03:33:25Z-
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