Sleep quality and preclinical Alzheimer Disease

By Yo-El S Ju, Jennifer McLeland, Cristina D. Toedebusch, C. Xiong, Anne M. Fagan, S. Duntley, John C. Morris, D. Holtzman. JAMA Neurology, 2013

685 citations recorded by the source corpus.

Objective Sleep and circadian problems are very common in Alzheimer Disease (AD). Recent animal studies suggest a bidirectional relationship between sleep and amyloid-β (Aβ), a key molecule involved in AD pathogenesis. This study tested whether Aβ deposition in preclinical AD, prior to the appearance of cognitive impairment, is associated with changes in quality or quantity of sleep. Methods Cognitively normal, middle-aged individuals (n=142) had sleep objectively measured using actigraphy for 2 weeks. Concurrent sleep diaries provided nap information. Cerebrospinal fluid Aβ42 levels were used to determine whether amyloid deposition was present or absent. Sleep parameters were assessed with regard to amyloid deposition. Results Amyloid deposition was associated with worse sleep quality, specifically worse sleep efficiency (% time in bed that was spent asleep), compared to those without amyloid deposition. In contrast, quantity of sleep was not different between groups, as measured by total sleep time. Frequent napping was associated with amyloid deposition. Interpretation Amyloid deposition in the preclinical stage of AD appears to be associated with worse sleep quality, but not with changes in sleep quantity.

Subfields: Cognitive Neuroscience, Endocrine and Autonomic Systems, Experimental and Cognitive Psychology

View Paper: https://www.semanticscholar.org/paper/949bbe137e9cde2826b1a8c1e2d9abf9b823ee1a

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Citations in the corpus

β-Amyloid accumulation in the human brain after one night of sleep deprivation (2018, background): “This association has been considered bidirectional because increased ABB could also lead to impairments in sleep (9, 10).”
New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation (2018, background): “Aβ plaques accumulate in the brains of AD patients’ years before the onset of cognitive impairment and serve as an early biomarker of AD (Ju et al., 2013).”
The Glymphatic System – A Beginner's Guide (2015, positive): “Moreover, work from David Holtzman documents that the concentration of b-amyloid in CSF follows the sleep-wake cycle in human subjects [132].”