Effect of sleep on overnight cerebrospinal fluid amyloid β kinetics

Brendan P. Lucey, Terry J. Hicks, Jennifer S. McLeland, Cristina D. Toedebusch, Jill Boyd, Donald L. Elbert, Bruce W. Patterson, Jack Baty, John C. Morris, Vitaliy Ovod, Kwasi G. Mawuenyega, Randall J. Bateman. Annals of Neurology, Volume 83, Issue 1, January 2018, Pages 197-204 Read More

Abstract

Sleep disturbances are associated with future risk of Alzheimer disease. Disrupted sleep increases soluble amyloid β, suggesting a mechanism for sleep disturbances to increase Alzheimer disease risk. We tested this response in humans using indwelling lumbar catheters to serially sample cerebrospinal fluid while participants were sleep-deprived, treated with sodium oxybate, or allowed to sleep normally. All participants were infused with 13C6-leucine to measure amyloid β kinetics. We found that sleep deprivation increased overnight amyloid β38, amyloid β40, and amyloid β42 levels by 25 to 30% via increased overnight amyloid β production relative to sleeping controls. These findings suggest that disrupted sleep increases Alzheimer disease risk via increased amyloid β production. Ann Neurol 2018;83:197–204. © 2017 American Neurological Association

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Posted on February 7, 2018
Posted in: HPAN, Neurodegeneration, Neurogenetics & Transcriptomics, Publications Authors: , ,