Evidence map›Paper›PMID 42335020›Full record

Trial reportPLoS biology2026

Sleep deprivation increases levels of the synaptic density marker SV2A in the human brain.

David Elmenhorst, Anna L Foerges, Ali Gordji-Nejad, Eva-Maria Elmenhorst, Tina Kroll, Andreas Matusch, Simone Beer, Bernd Neumaier, Philipp Krapf, Christoph Lerche and 2 more

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in PLoS biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

David ElmenhorstInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.ORCID https://orcid.org/0000-0001-6137-416X
Anna L FoergesInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Ali Gordji-NejadInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Eva-Maria ElmenhorstInstitute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany.
Tina KrollInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Andreas MatuschInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Simone BeerInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Bernd NeumaierInstitute of Neuroscience and Medicine (INM-5), Forschungszentrum Jülich, Jülich, Germany.
Philipp KrapfInstitute of Neuroscience and Medicine (INM-5), Forschungszentrum Jülich, Jülich, Germany.
Christoph LercheInstitute of Neuroscience and Medicine (INM-4), Forschungszentrum Jülich, Jülich, Germany.
Alexander DrzezgaInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.
Andreas BauerInstitute of Neuroscience and Medicine (INM-2), Forschungszentrum Jülich, Jülich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sleep is essential for synaptic homeostasis, a proposed mechanism whereby wakefulness leads to synaptic potentiation and sleep facilitates synaptic down-selection. Synaptic vesicle glycoprotein 2A (SV2A), whose availability is quantifiable by [¹⁸F]SynVesT-1 positron emission tomography (PET), is commonly interpreted as a proxy for synaptic density. In this randomized study, we examined 40 healthy adults (mean age 27.5 ± 6.5 years) who underwent two [¹⁸F]SynVesT-1 PET scans on consecutive days. Half of the participants were assigned to the normal sleep (i.e., control) condition and half to the sleep deprivation condition. Scans were performed at the same circadian time point, approximately 4 h after awakening in the control group and during baseline in the sleep deprivation group or after ~28 h of continuous wakefulness in the sleep deprivation group after sleep deprivation. Sleep deprivation led to significant increases in synaptic vesicle glycoprotein 2A binding in multiple brain regions, including the thalamus (+4.6%), hippocampus (+5.6%), and parietal cortex (+3.2%), whereas no changes were observed in controls. The degree of increase in synaptic vesicle glycoprotein 2A positively correlated with elevated slow wave activity during recovery sleep, a physiological marker of sleep pressure. These findings provide in vivo support for the synaptic homeostasis hypothesis in humans and suggest that synaptic vesicle glycoprotein 2A PET imaging is sensitive to sleep-wake dependent synaptic plasticity.

trial registrationThe study was prospectively registered on 19.01.2022 here: German Clinical Trials Registry: DRKS # DRKS00027867, https://drks.de/search/en/trial/DRKS00027867.

Indexed as

BrainMembrane GlycoproteinsNerve Tissue ProteinsSleep DeprivationAdultBiomarkersFemaleHumansMalePositron-Emission TomographySleepSynapsesWakefulnessYoung AdultBiomarkersMembrane GlycoproteinsNerve Tissue ProteinsSV2A protein, human

Identifiers

PMID42335020
PMCPMC13289872

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Registered trials

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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.