Effect of 1 Night of Total Sleep Deprivation on Cerebrospinal Fluid β-Amyloid 42 in Healthy Middle-Aged Men: A Randomized Clinical Trial
Open accessAbstract
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 β-amyloid (Aβ), which is a key protein in Alzheimer disease pathology. OBJECTIVE: To determine the effect of 1 night of total sleep deprivation on cerebrospinal fluid Aβ42 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 Aβ42 concentrations between evening and morning. RESULTS: A night of unrestricted sleep led to a 6% decrease in Aβ42 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 Aβ42 over time, a difference of 75.8 pg/mL of Aβ42 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 Aβ42 concentrations differed between the unrestricted sleep and sleep deprivation groups (P = .04) in contrast to stable Aβ40, tau, and total protein levels. CONCLUSIONS AND RELEVANCE: Sleep deprivation, or prolonged wakefulness, interferes with a physiological morning decrease in Aβ42. We hypothesize that chronic sleep deprivation increases cerebral Aβ42 levels, which elevates the risk of Alzheimer disease. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01194713.
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Impaired amyloidβ clearance usually occurs during deep sleep at the beginning of the night, which lasts one to two hours, so is unlikely to be affected in those reporting sleep disturbances.
“However, this usually occurs during deep sleep at the beginning of the night, which lasts one to two hours so is unlikely to be affected in those reporting sleep disturbances. (316-318)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [316]
The Discussion (page unavailable) links sleep to a decrease in CSF Aβ42 but does not place amyloid clearance exclusively in the first one to two hours of deep sleep. Contrary to the claim that sleep disturbances are unlikely to affect it, the Discussion reports that total sleep deprivation abolished the decrease, and the Conclusions hypothesize that disrupted sleep might contribute to Aβ42 accumulation. (LLM, conf=0.87)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredIn humans, SD increases CSF levels of Aβ38, Aβ40, and Aβ42 through enhancement of Aβ production.
“In humans, SD increases CSF levels of Aβ38, Aβ40, and Aβ42 through the enhancement of Aβ production [568, 569].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [568]
A single night of sleep deprivation elevates CSF Aβ42 in healthy middle-aged men.
“A single night of sleep deprivation leads to elevated CSF Aβ42 levels in healthy middle-aged men (Ooms et al., 2014).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Ooms et al., 2014
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- Authors
- Ooms, S., Overeem, S., Besse, K., Rikkert, M. O., Verbeek, M., & Claassen, J. A. H. R.
- Affiliations
- Radboud University Nijmegen (NL)
- Donders Institute for Brain, Cognition, and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands2Radboud Alzheimer Center, Radboud University Medical Center, Nijmegen, the Netherlands3Department of Geriatric Medicine, Radboud University
- Corresponding author
- Claassen, Jurgen A. H. R.
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2014-08-01
- Volume
- 71
- Issue
- 8
- Pages
- 971
- ISSN
- 2168-6149 (ISSN-L)
- OpenAlex
- W2160311930
- Cited by
- 438
- References
- 30
- Citations by year
- 2026: 33 · 2025: 45 · 2024: 53 · 2023: 36 · 2022: 32 · 2021: 49 · 2020: 51 · 2019: 42 · 2018: 27 · 2017: 30 · 2016: 14 · 2015: 20 · 2014: 5
- FWCI
- 12.83
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- JAMA Neurology (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- TU/e Research Portal (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Keywords
- total sleep deprivation, amyloid-beta 42, cerebrospinal fluid, Alzheimer's disease risk, prolonged wakefulness, circadian rhythm, amyloid clearance, middle-aged men, tau protein, Aβ40, polysomnography, cognitive aging
- MeSH terms
- Adult, Humans, Male, Middle Aged, Peptide Fragments, Sleep, Sleep Deprivation, Time Factors, Amyloid beta-Peptides, Polysomnography
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