{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T06:32:02Z","timestamp":1789713122060,"version":"4.0.1"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T00:00:00Z","timestamp":1702339200000},"content-version":"vor","delay-in-days":345,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Acute sleep deprivation has been shown to affect cerebrospinal fluid and plasma concentrations of biomarkers associated with neurodegeneration, though the mechanistic underpinnings remain unknown. This study compared individuals who, for one night, were either subject to total sleep deprivation or free sleep, (i) examining plasma concentrations of neurodegeneration biomarkers the morning after sleep deprivation or free sleep and (ii) determining how overnight changes in biomarkers plasma concentrations correlate with indices of meningeal lymphatic and glymphatic clearance functions. Plasma concentrations of amyloid-\u03b2 40 and 42, phosphorylated tau peptide 181, glial fibrillary acid protein and neurofilament light were measured longitudinally in subjects who from Day 1 to Day 2 either underwent total sleep deprivation (n = 7) or were allowed free sleep (n = 21). The magnetic resonance imaging contrast agent gadobutrol was injected intrathecally, serving as a cerebrospinal fluid tracer. Population pharmacokinetic model parameters of gadobutrol cerebrospinal fluid-to-blood clearance were utilized as a proxy of meningeal lymphatic clearance capacity and intrathecal contrast-enhanced magnetic resonance imaging as a proxy of glymphatic function. After one night of acute sleep deprivation, the plasma concentrations of amyloid-\u03b2 40 and 42 were reduced, but not the ratio, and concentrations of the other biomarkers were unchanged. The overnight change in amyloid-\u03b2 40 and 42 plasma concentrations in the sleep group correlated significantly with indices of meningeal lymphatic clearance capacity, while this was not seen for the other neurodegeneration biomarkers. However, overnight change in plasma concentrations of amyloid-\u03b2 40 and 42 did not correlate with the glymphatic marker. On the other hand, the overnight change in plasma concentration of phosphorylated tau peptide 181 correlated significantly with the marker of glymphatic function in the sleep deprivation group but not in the sleep group. The present data add to the evidence of the role of sleep and sleep deprivation on plasma neurodegeneration concentrations; however, the various neurodegeneration biomarkers respond differently with different mechanisms behind sleep-induced alterations in amyloid-\u03b2 and tau plasma concentrations. Clearance capacity of meningeal lymphatics seems more important for sleep-induced changes in amyloid-\u03b2 40 and 42 plasma concentrations, while glymphatic function seems most important for change in plasma concentration of phosphorylated tau peptide 181 during sleep deprivation. Altogether, the present data highlight diverse mechanisms behind sleep-induced effects on concentrations of plasma neurodegeneration biomarkers.<\/jats:p>","DOI":"10.1093\/braincomms\/fcad343","type":"journal-article","created":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T22:50:49Z","timestamp":1702421449000},"source":"Crossref","is-referenced-by-count":25,"title":["Mechanisms behind changes of neurodegeneration biomarkers in plasma induced by sleep deprivation"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6881-9280","authenticated-orcid":false,"given":"Per Kristian","family":"Eide","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Oslo University Hospital\u2014Rikshospitalet , N-0424 Oslo , Norway"},{"name":"Institute of Clinical Medicine, Faculty of Medicine, University of Oslo , N-0316 Oslo , Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aslan","family":"Lashkarivand","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Oslo University Hospital\u2014Rikshospitalet , N-0424 Oslo , Norway"},{"name":"Institute of Clinical Medicine, Faculty of Medicine, University of Oslo , N-0316 Oslo , Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Are Hugo","family":"Pripp","sequence":"additional","affiliation":[{"name":"Oslo Centre of Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital , N-0424 Oslo , Norway"},{"name":"Faculty of Health Sciences, Oslo Metropolitan University , N-0130 Oslo , Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars Magnus","family":"Valnes","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Oslo University Hospital\u2014Rikshospitalet , N-0424 Oslo , 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Physiology, the Sahlgrenska Academy at the University of Gothenburg , S-405 30 Gothenburg , Sweden"},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , S-405 30 Gothenburg , Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3930-4354","authenticated-orcid":false,"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , S-405 30 Gothenburg , Sweden"},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , S-405 30 Gothenburg , Sweden"},{"name":"Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square , London WC1E 6BT , UK"},{"name":"UK Dementia Research Institute at UCL , London WC1E 6BT , UK"},{"name":"Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay , Hong Kong 999077 , 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