Effect of 1 night of total sleep deprivation on cerebrospinal fluid beta-amyloid 42 in healthy middle-aged men: a randomized clinical trial
until further notice
SourceJama Neurology, 71, 8, (2014), pp. 971-977
Article / Letter to editor
Display more detailsDisplay less details
SubjectRadboudumc 1: Alzheimer`s disease DCMN: Donders Center for Medical Neuroscience; Radboudumc 3: Disorders of movement DCMN: Donders Center for Medical Neuroscience
IMPORTANCE: Increasing evidence suggests a relationship between poor sleep and the risk of developing Alzheimer disease. A previous study found an effect of sleep on beta-amyloid (Abeta), which is a key protein in Alzheimer disease pathology. OBJECTIVE: To determine the effect of 1 night of total sleep deprivation on cerebrospinal fluid Abeta42 protein levels in healthy middle-aged men. DESIGN, SETTING, AND PARTICIPANTS: The Alzheimer, Wakefulness, and Amyloid Kinetics (AWAKE) study at the Radboud Alzheimer Center, a randomized clinical trial that took place between June 1, 2012, and October 1, 2012. Participants were cognitively normal middle-aged men (40-60 years of age) with normal sleep (n = 26) recruited from the local population. INTERVENTIONS: Participants were randomized to 1 night with unrestricted sleep (n = 13) or 1 night of total sleep deprivation (24 hours of wakefulness) (n = 13). MAIN OUTCOMES AND MEASURES: Sleep was monitored using continuous polysomnographic recording from 3 pm until 10 am. Cerebrospinal fluid samples were collected using an intrathecal catheter at defined times to compare cerebral Abeta42 concentrations between evening and morning. RESULTS: A night of unrestricted sleep led to a 6% decrease in Abeta42 levels of 25.3 pg/mL (95% CI [0.94, 49.6], P = .04), whereas sleep deprivation counteracted this decrease. When accounting for the individual trajectories of Abeta42 over time, a difference of 75.8 pg/mL of Abeta42 was shown between the unrestricted sleep and sleep deprivation group (95% CI [3.4, 148.4], P = .04). The individual trajectories of evening and morning Abeta42 concentrations differed between the unrestricted sleep and sleep deprivation groups (P = .04) in contrast to stable Abeta40, tau, and total protein levels. CONCLUSIONS AND RELEVANCE: Sleep deprivation, or prolonged wakefulness, interferes with a physiological morning decrease in Abeta42. We hypothesize that chronic sleep deprivation increases cerebral Abeta42 levels, which elevates the risk of Alzheimer disease. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01194713.
Upload full text
Use your RU credentials (u/z-number and password) tolog in with SURFconextto upload a file for processing by the repository team.