Sleep duration, sleep efficiency, and amyloid ß among cognitively healthy later-life adults: a systematic review and meta-analysis.

BACKGROUND: Abnormal amyloid ß (Aß) deposits in the brain are a hallmark of Alzheimer's disease (AD). Insufficient sleep duration and poor sleep quality are risk factors for developing AD. Sleep may play a role in Aß regulation, but the magnitude of the relationship between sleep and Aß deposition remains unclear. This systematic review examines the relationship between sleep (i.e., duration and efficiency) with Aß deposition in later-life adults. METHODS: A search of PubMed, CINAHL, Embase, and PsycINFO generated 5,005 published articles. Fifteen studies met the inclusion criteria for qualitative syntheses; thirteen studies for quantitative syntheses related to sleep duration and Aß; and nine studies for quantitative syntheses related to sleep efficiency and Aß. RESULTS: Mean ages of the samples ranged from 63 to 76 years. Studies measured Aß 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 measured subjectively using interviews or questionnaires, or objectively using polysomnography or actigraphy. Study analyses accounted for demographic and lifestyle factors. Based on 13 eligible articles, our synthesis demonstrated that the average association between sleep duration and Aß was not statistically significant (Fisher's Z = -0.055, 95% CI = -0.117 ~ 0.008). We found that longer self-report sleep duration is associated with lower Aß (Fisher's Z = -0.062, 95% CI = -0.119 ~ -0.005), whereas the objectively measured sleep duration was not associated with Aß (Fisher's Z = 0.002, 95% CI = -0.108 ~ 0.113). Based on 9 eligible articles for sleep efficiency, our synthesis also demonstrated that the average association between sleep efficiency and Aß was not statistically significant (Fisher's Z = 0.048, 95% CI = -0.066 ~ 0.161). CONCLUSION: The findings from this review suggest that shorter self-reported sleep duration is associated with higher Aß levels. Given the heterogeneous nature of the sleep measures and outcomes, it is still difficult to determine the exact relationship between sleep and Aß. Future studies with larger sample sizes should focus on comprehensive sleep characteristics and use longitudinal designs to better understand the relationship between sleep and AD.

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

Background: Amyloid ß (Aß) 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 Aß. However, the magnitude of the relationship between sleep duration and Aß is still unclear. This systematic review examines the relationship between sleep duration and Aß 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 Aß 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 Aß. Using seven eligible articles, our quantitative synthesis demonstrated that the average association between sleep duration and Aß 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 Aß 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.