Acute Sleep Deprivation Increases Serum Levels of Neuron-Specific Enolase (NSE) and S100 Calcium Binding Protein B (S-100B) in Healthy Young Men

Benedict, Christian; Cedernaes, Jonathan; Giedraitis, Vilmantas; Nilsson, Emil; Hogenkamp, Pleunie S.; Vågesjö, Evelina; Massena, Sara; Pettersson, Ulrika; Christoffersson, Gustaf; Phillipson, Mia; Broman, Jan‐Erik; Lannfelt, Lars; Zetterberg, Henrik; Schiöth, Helgi B.

doi:10.5665/sleep.3336

Cited by 71 publications

(48 citation statements)

References 20 publications

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“…The increased blood–brain barrier permeability during sleep loss may explain the findings by Benedict et al . (), regarding the presence of neuronal and glial proteins in plasma after acute sleep deprivation in humans (Benedict et al ., ). The prolonged blood–brain barrier hyperpermeability after sleep loss might underlie the effects of sleep loss in hippocampal physiology, such as decreased neurogenesis (Guzmán‐Marín et al ., : Mueller et al ., ), altered hippocampal neurochemistry (Mohammed et al ., ) and reduced hippocampal volume (Meerlo et al ., ; Novati et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Chronic sleep restriction disrupts interendothelial junctions in the hippocampus and increases blood–brain barrier permeability

Hurtado‐Alvarado

Velázquez‐Moctezuma

Gómez-González

2017

Journal of Microscopy

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Chronic sleep loss in the rat increases blood-brain barrier permeability to Evans blue and FITC-dextrans in almost the whole brain and sleep recovery during short periods restores normal blood-brain barrier permeability. Sleep loss increases vesicle density in hippocampal endothelial cells and decreases tight junction protein expression. However, at the ultrastructural level the effect of chronic sleep loss on interendothelial junctions is unknown. In this study we characterised the ultrastructure of interendothelial junctions in the hippocampus, the expression of tight junction proteins, and quantified blood-brain barrier permeability to fluorescein-sodium after chronic sleep restriction. Male Wistar rats were sleep restricted using the modified multiple platform method during 10 days, with a daily schedule of 20-h sleep deprivation plus 4-h sleep recovery at their home-cages. At the 10th day hippocampal samples were obtained immediately at the end of the 20-h sleep deprivation period, and after 40 and 120 min of sleep recovery. Samples were processed for transmission electron microscopy and western blot. Chronic sleep restriction increased blood-brain barrier permeability to fluorescein-sodium, and decreased interendothelial junction complexity by increasing the frequency of less mature end-to-end and simply overlap junctions, even after sleep recovery, as compared to intact controls. Chronic sleep loss also induced the formation of clefts between narrow zones of adjacent endothelial cell membranes in the hippocampus. The expression of claudin-5 and actin decreased after chronic sleep loss as compared to intact animals. Therefore, it seems that chronic sleep loss disrupts interendothelial junctions that leads to blood-brain barrier hyperpermeability in the hippocampus.

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Section: Discussionmentioning

confidence: 99%

Chronic sleep restriction disrupts interendothelial junctions in the hippocampus and increases blood–brain barrier permeability

Hurtado‐Alvarado

Velázquez‐Moctezuma

Gómez-González

2017

Journal of Microscopy

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“…This experiment was a component of a larger study investigating a variety of other measures related to sleep deprivation's impact on hunger levels and immune system functioning, and thus parts of the study have been reported previously . Data regarding ghrelin levels was also reported in a previous paper .…”

Section: Methodsmentioning

confidence: 99%

Acute sleep deprivation increases food purchasing in men

Chapman

Nilsson

et al. 2013

Obesity

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Objective: To investigate if acute sleep deprivation affects food purchasing choices in a mock supermarket. Design and Methods: On the morning after one night of total sleep deprivation (TSD) or after one night of sleep, 14 normal-weight men were given a fixed budget (300 SEK-approximately 50 USD). They were instructed to purchase as much as they could out of a possible 40 items, including 20 high-caloric foods (>2 kcal/g) and 20 low-caloric foods (<2 kcal/g). The prices of the high-caloric foods were then varied (75%, 100% (reference price), and 125%) to determine if TSD affects the flexibility of food purchasing. Before the task, participants received a standardized breakfast, thereby minimizing the potential confound produced by hunger. In addition, morning plasma concentrations of the orexigenic hormone ghrelin were measured under fasting conditions. Results: Independent of both type of food offered and price condition, sleep-deprived men purchased significantly more calories (19%) and grams (118%) of food than they did after one night of sleep (both P < 0.05). Morning plasma ghrelin concentrations were also higher after TSD (P < 0.05). However, this increase did not correlate with the effects of TSD on food purchasing. Conclusions: This experiment demonstrates that acute sleep loss alters food purchasing behavior in men.Obesity (2013) 21, E555-E560.

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“…Mouse models of AD, PD, and HD pathology also exhibit sleep abnormalities (21–24). Sleep deprivation increases cerebrospinal fluid markers of neuronal injury and alters plasma markers of inflammation in humans (25, 26), and induces the unfolded protein response in the brain of mice, indicating endoplasmic reticulum stress and potential neuronal injury (27). Thus, inadequate sleep could prime the brain for neurodegeneration by promoting processes such as inflammation and synaptic damage which exert pathogenic effects across diseases.…”

Section: Sleep and Neurodegenerationmentioning

confidence: 99%

Mechanisms linking circadian clocks, sleep, and neurodegeneration

Musiek

Holtzman

2016

Science

616

498

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Disruption of normal circadian rhythms and sleep cycles are consequences of aging and can profoundly impact health. Accumulating evidence indicates that circadian and sleep disturbances, which have long been considered symptoms of many neurodegenerative conditions, may actually drive pathogenesis early in the course of these diseases. In this review we explore potential cellular and molecular mechanisms linking circadian dysfunction and sleep loss to neurodegenerative diseases, with a focus on Alzheimer’s Disease. We examine the interplay between central and peripheral circadian rhythms, circadian clock gene function, and sleep in maintaining brain homeostasis, and discuss therapeutic implications. The circadian clock and sleep can influence a number of key processes involved in neurodegeneration, suggesting that these systems might be manipulated to promote healthy brain aging.

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Acute Sleep Deprivation Increases Serum Levels of Neuron-Specific Enolase (NSE) and S100 Calcium Binding Protein B (S-100B) in Healthy Young Men

Cited by 71 publications

References 20 publications

Chronic sleep restriction disrupts interendothelial junctions in the hippocampus and increases blood–brain barrier permeability

Chronic sleep restriction disrupts interendothelial junctions in the hippocampus and increases blood–brain barrier permeability

Acute sleep deprivation increases food purchasing in men

Mechanisms linking circadian clocks, sleep, and neurodegeneration

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