Evidence map›Paper›PMID 40830882›Full record

Trial reportFluids and barriers of the CNS2025

Sleep reduces CSF concentrations of beta-amyloid and tau: a randomized crossover study in healthy adults.

Tim Lyckenvik, Martin Olsson, My Forsberg, Pontus Wasling, Henrik Zetterberg, Jan Hedner, Eric Hanse

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Fluids and barriers of the CNS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Tim Lyckenvik *Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. tim.lyckenvik@gu.se.
Martin Olsson *Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
My ForsbergDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Pontus WaslingDepartment of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Jan HednerDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Eric HanseDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSlow-wave sleep has been proposed to facilitate the removal of proteins, implicated in neurodegeneration, from the brain. While mechanistic evidence from animal models is accumulating, direct human data on how slow-wave sleep shapes cerebrospinal fluid (CSF) proteostasis remain limited, constraining our understanding of physiological resilience to neurodegenerative disease.

methodsTwelve healthy adults (aged 20–40 years) underwent CSF sampling following three controlled sleep conditions in a randomized crossover design; (1) one night of sleep followed by afternoon CSF sampling, (2) one night of sleep followed by morning CSF sampling, and (3) one night of total sleep deprivation followed by morning CSF sampling. Sleep and wakefulness were verified using polysomnography and actigraphy, with > 4-week washout periods between conditions. Measured CSF biomarkers included Alzheimer’s disease-related proteins: beta-amyloid isoforms (Aβ38, Aβ40, and Aβ42), total tau, tau phosphorylated at amino acid 181 (p-tau), glial fibrillary acidic protein (GFAP), and neurofilament light chain, as well as orexin, albumin (also measured in serum), and osmolality. Differences between conditions were assessed using Friedman tests with Dunn’s post hoc correction.

resultsCSF levels of Aβ and tau tended to be consistently lower after sleep compared with both afternoon sampling and post-sleep deprivation. Concurrently, CSF albumin levels increased after sleep, while neurofilament light and GFAP remained unchanged. Orexin levels rose markedly during sleep deprivation but showed no circadian variation and did not track with biomarker levels.

conclusionsThese findings support a model in which slow-wave sleep selectively reduces CSF concentrations of Aβ and tau, potentially through enhanced solute mobility and receptor-mediated clearance. Unchanged levels of NfL and GFAP argue against bulk clearance. Orexin may primarily function to oppose sleep pressure rather than directly regulate proteostasis. These hypotheses merit direct testing to inform strategies for delaying pathological protein accumulation in neurodegenerative disease.

Indexed as

Amyloid beta-PeptidesPeptide FragmentsSleepSleep DeprivationSleep, Slow-Wavetau ProteinsAdultBiomarkersCross-Over StudiesFemaleGlial Fibrillary Acidic ProteinHumansMaleNeurofilament ProteinsOrexinsPolysomnographyAmyloid beta-PeptidesBiomarkersGlial Fibrillary Acidic ProteinMAPT protein, humanNeurofilament ProteinsOrexinsPeptide Fragmentstau ProteinsAlzheimer’s diseaseAmyloid betaSleepSlow wave sleepTau

Identifiers

PMID40830882
PMCPMC12366049

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.