Journal Article

FZJ-2026-02877

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Sleep deprivation increases levels of the synaptic density marker SV2A in the human brain

Elmenhorst, D. (Corresponding author)FZJ* ; Foerges, A. L.FZJ* ; Gordji-Nejad, A.FZJ* ; Elmenhorst, E.-M. ; Kroll, T.FZJ* ; Matusch, A.FZJ* ; Beer, S.FZJ* ; Neumaier, B.FZJ* ; Krapf, P.FZJ* ; Lerche, C.FZJ* ; Drzezga, A.FZJ* ; Bauer, A.FZJ*

2026
PLoS Lawrence, KS

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Please use a persistent id in citations: doi:10.1371/journal.pbio.3003816  doi:10.34734/FZJ-2026-02877

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 sleepwake dependent synaptic plasticity.

Note: This research was supported by internal institutional funds and the project SleepLess, which received funding from the Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research, BMBF), the Fonds voor Wetenschappelijk Onderzoek - Research Foundation Flanders (FWO), and the Fonds de recherche du Québec - Santé (Quebec Health Research Fund, FRQS) under the frame of ERA-NET Neuron Cofund (grant # 01EW1808). AD received funding from public funding authorities: German Research Foundation (Grants for Collaborative Research Centre 1451 C04 and DR 445/9-1) and Wellcome Leap. The funders did not play any role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript

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Contributing Institute(s):

1. Nuklearchemie (INM-5)
2. Physik der Medizinischen Bildgebung (INM-4)
3. Molekulare Organisation des Gehirns (INM-2)

Research Program(s):

1. 5253 - Neuroimaging (POF4-525) (POF4-525)

Appears in the scientific report 2026

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