2020-nedergaard.pdf: “Glymphatic failure as a final common pathway to dementia”, (2020-10-02):
Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. Sleep quality decreases as we age, and disruption of the regular sleep architecture is a frequent antecedent to the onset of dementia in neurodegenerative diseases. The glymphatic system, which clears the brain of protein waste products, is mostly active during sleep. Yet the glymphatic system degrades with age, suggesting a causal relationship between sleep disturbance and symptomatic progression in the neurodegenerative dementias. The ties that bind sleep, aging, glymphatic clearance, and protein aggregation have shed new light on the pathogenesis of a broad range of neurodegenerative diseases, for which glymphatic failure may constitute a therapeutically targetable final common pathway.
2020-vaccaro.pdf: “Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut”, (2020-06-11):
- Sleep deprivation leads to ROS accumulation in the fly and mouse gut
- Gut-accumulated ROS trigger oxidative stress in this organ
- Preventing ROS accumulation in the gut allows survival without sleep in flies
Abstract: The view that sleep is essential for survival is supported by the ubiquity of this behavior, the apparent existence of sleep-like states in the earliest animals, and the fact that severe sleep loss can be lethal. The cause of this lethality is unknown. Here we show, using flies and mice, that sleep deprivation leads to accumulation of reactive oxygen species (ROS) and consequent oxidative stress, specifically in the gut. ROS are not just correlates of sleep deprivation but drivers of death: their neutralization prevents oxidative stress and allows flies to have a normal lifespan with little to no sleep. The rescue can be achieved with oral antioxidant compounds or with gut-targeted transgenic expression of antioxidant enzymes. We conclude that death upon severe sleep restriction can be caused by oxidative stress, that the gut is central in this process, and that survival without sleep is possible when ROS accumulation is prevented.
[Keywords: sleep, sleep deprivation, reactive oxygen species, oxidative stress, free radicals, gut, survival, antioxidants]
2017-boland.pdf: “Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation”, Elaine M. Boland, Hengyi Rao, David F. Dinges, Rachel V. Smith, Namni Goel, John A. Detre, Mathias Basner, Yvette I. Sheline, Michael E. Thase, Philip R. Gehrman ( )
2013-zeo-exportdatasheet.pdf: “Zeo_DataDownload™_Help_Sheet”, Emily Tata ( )
2013-tonetti.pdf: “Polysomnographic validation of a wireless dry headband technology for sleep monitoring in healthy young adults”, Lorenzo Tonetti, Nicola Cellini, Massimiliano de Zambotti, Marco Fabbri, Monica Martoni, Stephan E. Fábregas, Luciano Stegagno, Vincenzo Natale ( )
2013-cajochen.pdf: “Evidence that the Lunar Cycle Influences Human Sleep”, Christian Cajochen, Songül Altanay-Ekici, Mirjam Münch, Sylvia Frey, Vera Knoblauch, Anna Wirz-Justice ( )
2012-gominak.pdf: “The world epidemic of sleep disorders is linked to vitamin D deficiency”, S. C. Gominak, W. E. Stumpf ( )
2011-sato-mito.pdf: “The midpoint of sleep is associated with dietary intake and dietary behavior among young Japanese women”, Natsuko Sato-Mito, Satoshi Sasaki, Kentaro Murakami, Hitomi Okubo, Yoshiko Takahashi, Shigenobu Shibata, Kazuhiko Yamada, Kazuto Sato, the Freshmen in Dietetic Courses Study II group ( )
2010-drake.pdf: “Untitled”, Allison Sheridan ( )
2007-trajanovic.pdf: “Positive sleep state misperception – A new concept of sleep misperception”, Nikola N. Trajanovic, Vlada Radivojevic, Yulia Kaushansky, Colin M. Shapiro
2006-tononi.pdf: “Sleep function and synaptic homeostasis”, (2006-02-01; ):
This paper reviews a novel hypothesis about the functions of slow wave sleep—the synaptic homeostasis hypothesis. According to the hypothesis, plastic processes occurring during wakefulness result in a net increase in synaptic strength in many brain circuits. The role of sleep is to downscale synaptic strength to a baseline level that is energetically sustainable, makes efficient use of gray matter space, and is beneficial for learning and memory. Thus, sleep is the price we have to pay for plasticity, and its goal is the homeostatic regulation of the total synaptic weight impinging on neurons. The hypothesis accounts for a large number of experimental facts, makes several specific predictions, and has implications for both sleep and mood disorders.
[Keywords: Long-term depression, Synaptic scaling, Learning, Consolidation, Delta sleep, Slow waves, Slow oscillation]
1997-wyatt.pdf: “Mesograde Amnesia During the Sleep Onset Transition: Replication and Electrophysiological Correlates”, James K. Wyatt, Richard R. Bootzin, John J. B. Allen, Jennifer L. Anthony