Slow wave sleep disruption increases cerebrospinal fluid amyloid-β levels
Open accessAbstract
See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article.Sleep deprivation increases amyloid-β, suggesting that chronically disrupted sleep may promote amyloid plaques and other downstream Alzheimer's disease pathologies including tauopathy or inflammation. To date, studies have not examined which aspect of sleep modulates amyloid-β or other Alzheimer's disease biomarkers. Seventeen healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, followed by slow wave activity disruption during polysomnogram, and cerebrospinal fluid collection the following morning for measurement of amyloid-β, tau, total protein, YKL-40, and hypocretin. Data were compared to an identical protocol, with a sham condition during polysomnogram. Specific disruption of slow wave activity correlated with an increase in amyloid-β40 (r = 0.610, P = 0.009). This effect was specific for slow wave activity, and not for sleep duration or efficiency. This effect was also specific to amyloid-β, and not total protein, tau, YKL-40, or hypocretin. Additionally, worse home sleep quality, as measured by sleep efficiency by actigraphy in the six nights preceding lumbar punctures, was associated with higher tau (r = 0.543, P = 0.045). Slow wave activity disruption increases amyloid-β levels acutely, and poorer sleep quality over several days increases tau. These effects are specific to neuronally-derived proteins, which suggests they are likely driven by changes in neuronal activity during disrupted sleep.
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A study involving cognitively healthy adults showed that amyloid-beta in cerebrospinal fluid or the hippocampus increases after sleep deprivation or slow-wave sleep disruption.
“A study involving cognitively healthy adults showed that Aβ in CSF or the hippocampus increases after sleep deprivation or slow-wave sleep disruption, which indicates the complexity of Aβ kinetics [59, 60, 61].”
From Clinical trials of new drugs for Alzheimer disease (2020) · cites this paper as [59]
In all these diseases, deficient sleep is common.
“In all these diseases, deficient sleep is common (279).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [279]
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- Authors
- Ju, Y.-E. S., Ooms, S. J., Sutphen, C., Macauley, S. L., Zangrilli, M. A., Jerome, G., Fagan, A. M., Mignot, E., Zempel, J. M., Claassen, J. A. H. R., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Radboud University Medical Center (NL)
- Stanford University (US)
- Corresponding author
- Ju, Yo-El S
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-07-10
- Volume
- 140
- Issue
- 8
- Pages
- 2104-2111
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC5790144
- OpenAlex
- W2735226312
- Cited by
- 604
- References
- 34
- Citations by year
- 2026: 61 · 2025: 72 · 2024: 84 · 2023: 71 · 2022: 64 · 2021: 75 · 2020: 67 · 2019: 66 · 2018: 34 · 2017: 9
- FWCI
- 27.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institutes of Health (K23-NS089922, UL1RR024992, KL2-TR000450, P01NS074969, P01-AG026276, P01-NS074969, P01-AG03991)
- 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 related disorders
- Keywords
- slow-wave sleep, sleep disruption, amyloid-beta, cerebrospinal fluid biomarkers, Alzheimer's disease, tau protein, sleep quality, actigraphy, YKL-40, orexin, polysomnography, neuronal activity
- MeSH terms
- Orexins, Chitinase-3-Like Protein 1, Adult, Aged, Apolipoproteins E, Cerebrospinal Fluid Proteins, Female, Humans, Male, Middle Aged, Peptide Fragments, Sleep, Sleep Deprivation, Amyloid beta-Peptides, tau Proteins, Polysomnography, Actigraphy
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