Insomnia Moderates the Relationship Between Amyloid-ß and Cognitive Decline in Late-Life Adults without Dementia.

BACKGROUND: It is suggested that not all individuals with elevated Aß will develop dementia or cognitive impairment. Environment or lifestyle might modulate the association of amyloid pathology with cognition. Insomnia is a risk factor of cognitive disorders including Alzheimer's disease. OBJECTIVE: To investigate if insomnia moderated the relationship between amyloid-ß (Aß) and longitudinal cognitive performance in non-demented elders. METHODS: A total of 385 Alzheimer's Disease Neuroimaging Initiative participants (mean age = 73 years, 48% females) who completed 4 + neuropsychological evaluations and a [18F] florbetapir positron emission tomography scan were followed up to 8 years. Linear mixed-effects regression models were used to examine the interactions effect between insomnia and Aß on longitudinal cognitive sores, including four domains (memory [MEM], executive function [EF], language [LAN], and visuospatial function [VS]). RESULTS: The Aß-positive status (A+) but not insomnia independently predicted faster cognitive decline in all domains. Furthermore, the relationship between Aß and cognitive decline was moderated by insomnia (MEM: χ2 = 4.05, p = 0.044, EF: χ2 = 4.38, p = 0.036, LAN: χ2 = 4.56, p = 0.033, and VS: χ2 = 4.12, p = 0.042). Individuals with both elevated Aß and insomnia experienced faster cognitive decline than those with only elevated Aß or insomnia. CONCLUSION: These data reinforced the values of insomnia management in preventing dementia, possibly by interacting Aß metabolism. Future efforts are warranted to determine whether sleep improvement will postpone the onset of dementia, specifically among populations in stages of preclinical or prodromal AD.

Sleep problems and risk of all-cause cognitive decline or dementia: an updated systematic review and meta-analysis.

OBJECTIVES: To conduct an updated systematic review and meta-analysis of association between sleep and all-cause cognitive disorders. METHODS: PubMed and EMBASE were searched from inception to 18 February 2019. Cohort studies exploring longitudinal associations of sleep with cognitive decline or dementia were included. The multivariable-adjusted effect estimates were pooled by random-effects models, with credibility assessment. The robust error meta-regression model was used to conduct the dose-response meta-analysis for sleep duration. RESULTS: 11 155 reports were searched and 51 eligible cohorts with 15 sleep problems were included for our meta-analyses. Ten types of sleep conditions or parameters, including six (insomnia, fragmentation, daytime dysfunction, prolonged latency, rapid eye movement sleep behaviour disorder and excessive time in bed) with moderate-to-high levels of evidence, were linked to higher risk of all-cause cognitive disorders. Furthermore, a U-shaped relationship was revealed for the associations with sleep duration. CONCLUSIONS: Sleep management might serve as a promising target for dementia prevention.