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Sleep Duration and Amyloid β Among Cognitively Healthy Later-Life Adults: A Systematic Review and Meta-Analysis

BACKGROUND: Amyloid β (Aβ) is a hallmark of Alzheimer’s disease (AD). Insufficient sleep duration and poor sleep quality have been found to be a risk factor of developing AD because sleep may involve regulating Aβ. However, the magnitude of the relationship between sleep duration and Aβ is still unc...

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Detalles Bibliográficos
Autores principales: Moon, Chooza, Schneiner, Aaron, Cho, Young Eun, Zhang, Meina, Dang, Hellen, Vu, Kelly
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Journal Experts 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10153382/
https://www.ncbi.nlm.nih.gov/pubmed/37131764
http://dx.doi.org/10.21203/rs.3.rs-2782680/v1
Descripción
Sumario:BACKGROUND: Amyloid β (Aβ) is a hallmark of Alzheimer’s disease (AD). Insufficient sleep duration and poor sleep quality have been found to be a risk factor of developing AD because sleep may involve regulating Aβ. However, the magnitude of the relationship between sleep duration and Aβ is still unclear. This systematic review examines the relationship between sleep duration and Aβ in later-life adults. METHODS: We screened 5,005 published articles searched from relevant electronic databases (i.e., PubMed, CINAHL, Embase, and PsycINFO) and reviewed 14 articles for the qualitative synthesis and 7 articles for the quantitative synthesis. RESULTS: Mean ages of the samples ranged from 63 to 76. Studies measured Aβ using cerebrospinal fluid, serum, and positron emission tomography scans with two tracers: Carbone 11-labeled Pittsburgh compound B or fluorine 18–labeled. Sleep duration was subjectively measured using interviews, questionnaires, or using objective measures such as polysomnography or actigraphy. The studies accounted for demographic and lifestyle factors in their analyses. Five of the 14 studies reported a statistically significant association between sleep duration and Aβ. Using seven eligible articles, our quantitative synthesis demonstrated that the average association between sleep duration and Aβ was not statistically significant (Fisher’s Z = −0.006, 95% CI= −0.065 ~ 0.054). CONCLUSION: This review suggests that caution should be taken when considering sleep duration as the primary factor for Aβ levels. More studies are needed using a longitudinal design, comprehensive sleep metrics, and larger sample sizes to advance our understanding of the optimal sleep duration and AD prevention.