Search

Sleep is essential for the maintenance of human physical health (Grandner et al., 2012; Reid et al., 2006), cognitive performance (Ferrie et al., 2011; Leng et al., 2017), and mental health (Freeman et al., 2017; Joao et al., 2018). Experimental sleep deprivation and different degrees of sleep restriction permit the characterization of human sleep behaviors and brain's responses to inadequate sleep (Durmer and Dinges, 2005; Elmenhorst et al., 2017; Elmenhorst et al., 2018; Van Dongen et al., 2003). Sleep disruption is known to impact not only brain functions but also affects brain anatomy; earlier studies found that sleep deprivation is associated with lower volumes of gray matter across various brain regions (Åkerstedt et al., 2020; Liu et al., 2014; Long et al., 2020; Sun et al., 2020), however with inconsistent localization of effects. Other studies reported alterations in white matter microstructure (Elvsåshagen et al., 2015; Voldsbekk et al., 2021), increased ventricles size, and cognitive decline (Lo et al., 2014). In addition, one-night sleep deprivation was found to increase the Aβ burden in the right hippocampus and thalamus of healthy controls (Shokri-Kojori 2018), suggesting an interrupted clearance pathway due to sleep deprivation. These prior studies suggest that sleep deprivation may impact anatomical features of the brain, but there is a need for large-scale replications and extensions of previous work. Increased brain age compared to chronological age is a risk factor for several neurodegenerative and psychiatric disorders (Wyss-Coray, 2016). Brain-age prediction is a widely studied topic that aims to estimate the trajectory of brain aging (Franke et al., 2019), and its association with pathological conditions. MRI-derived features used to predict individuals’ brain age have proven to constitute a proxy for overall health (Habes et al., 2016, Koutsouleris et al., 2014, Cole et al., 2018). Sleep patterns also change with aging. In particular, older adults tend to sleep less, and present a more fragmented sleep with lower slow-wave sleep. They also present a reduced sleep rebound following sleep deprivation, report less sleepiness under acute sleep deprivation conditions, and report a smaller increase in lapses of attention after sleep deprivation [23]. However, little is known on whether brain-age models reflect the impact of sleep deprivation on the brain structure - i.e., the difference between predicted age and real age (so-called brain-age delta) using MRI data. We hypothesized that the morphological alterations associated with sleep deprivation would lead to an increased brain-delta score.

Poor sleep quality and sleep disorders, including obstructive sleep apnea and insomnia disorder, are considered important potential risk factors for cognitive decline and dementia, including Alzheimer's disease (AD). Potential reasons include sleep fragmentation, intermittent hypoxia, and immune dysfunction, which may precede lower Amyloid β (Aβ) clearance from the brain and increased Aβ and tau depositions (Emamian et al., 2016; Bucks et al., 2017; Xu et al., 2020). Sleep deprivation also affects the molecular signaling pathways in the hippocampus that are required for synaptic consolidation during memory formation (Havekes et al., 2017). Recently, the association between insufficient or excessive sleep duration (≤4 or ≥10 hours per night) and cognitive decline has been demonstrated in a large-scale study (Ma et al., 2020), suggesting that cognitive performance should be carefully monitored in individuals with short or long sleep duration. Similarly, another study assessing the link between sleep and cognitive performance in ∼500,000 older adults from the UK-Biobank revealed that abnormal sleep duration is linked to cognitive impairment (Kyle et al., 2017). In addition, the previous behavioral studies on the link between sleep and cognition have been mostly limited to the subjective assessment of sleep and are usually restricted to a population from a single country. Moreover, the neurobiological underpinnings of their association are still poorly understood. On the other hand, several studies have highlighted the key role of apolipoprotein E (APOE) ε4 on brain network connectivity, memory performance, and rate of cognitive decline in patients with minimal cognitive impairment (MCI), AD and cognitively unimpaired individuals. Thus, understanding the potential pathogenic link between sleep, APOE ε4, brain, and cognitive function might enable us to provide a model for earlier identification of people at increased risk of cognitive decline and dementia (Liu et al., 2013) that could be tested in future studies. Thus, the predictive role of objectively measured poor sleep quality on the cognitive performance of healthy adults, as well as the genetic and neurobiological mechanism of the interplay between sleep quality and cognitive functions, is still far from clear. To address these key questions on the road towards clinical translation, we propose a study to comprehensively assess the relationship between sleep, brain structure, APOE genotype, and cognitive functions in a large-scale worldwide population-based cohort throughout the ENIGMA-Sleep consortium (Tahmasian et al., 2021).

Objectives:Adenosine and cerebral adenosine A1 (A1AR) and A2A receptors are important modulators of the sleep-wake cycle and regulate to some extent the sleep-wake homeostasis. Acute sleep deprivation has been shown to result in an upregulation of A1ARs in human and rat brains. The stimulating effects of caffeine are evoked through non-selective antagonism at adenosine receptors. Using positron emission tomography (PET), we investigate the effect of repeated coffee consumption during chronic sleep restriction and subsequent coffee abstinence after recovery sleep on cerebral A1AR availability and occupancy in humans.Methods:Thirty healthy volunteers (28±5 years, 15f) completed an in-lab study including three [18F]CPFPX PET scans to determine cerebral A1AR availability after subsequent exposure to rested (3 nights with 8h time in bed (TIB)), chronically sleep restricted (5 nights with 5h TIB), and recovery (one night with 8h TIB) conditions. Participants either consumed freshly brewed coffee (n = 17) or decaffeinated coffee (n = 13) during 5 days of sleep restriction (prior caffeine abstinence > 10 days). Regular coffee contained 200 mg caffeine at 7.30 a.m. and 100 mg caffeine at 2.00 p.m., decaffeinated coffee contained 4 mg and 2 mg, respectively. PET scans were conducted at the same time of day under caffeine-abstinent rested conditions, roughly 7h after the latest coffee intake after sleep restriction, and after ~ 31h of coffee abstention after recovery. Caffeine levels in saliva were determined repeatedly. Cerebral A1AR availability was quantified by distribution volume (VT) and occupancy levels were calculated by applying the Lassen plot including cortical and subcortical areas, cerebellum, and pons.Results:In the decaffeinated coffee group, no differences in cerebral A1AR availability were found between baseline condition, 5 days of sleep restriction and one night of recovery sleep. Repeated administration of regular coffee resulted in a displacement of [18F]CPFPX binding of 19 ± 13 % on average. One day after coffee abstention and recovery sleep, VT values did not differ from baseline.Conclusions:Our data suggest that neither chronic sleep restriction for 5 days nor combination with repeated caffeine consumption result in a persistent change in the regulation of cerebral A1AR availability.Financial support:The work was supported by the Institute for Scientific Information on Coffee, the Swiss National Science Foundation (# 320030_163439) and respective institutional funds.

Field studies on traffic noise-induced annoyance have predominantly used estimated outside noise levels. We intended to complement existing knowledge with exposure–response relationships that are based on precise indoor noise measurements. Acoustic recordings inside the bedrooms of nightly road traffic and annoyance ratings in the following morning were obtained from 40 suburban residents (mean age 29.1 years ± 11.7, 26 females). We derived exposure–response functions for the probability to be “annoyed at least a little” (%LA). Further analyses compared data from the current study with those from two earlier studies on railway and aircraft noise. Annoyance increased with the number of traffic events and the equivalent sound pressure level. The inclusion of non-acoustical factors (such as assessment of road transport) improved the prediction considerably. When comparing the different traffic noise sources, %LA was higher for road than for air traffic at a given LAeq,night, but higher for road and railway than for air traffic at a given number of noise events. Acoustical as well as non-acoustical factors impact short-term annoyance induced by road, railway, and air traffic. Annoyance varies across noise sources, which may be due to differences in acoustical characteristics or in the temporal noise distribution throughout the night.

A sleep deprivation study was conducted at the German Aerospace Center (DLR) to examine the effects of sleepiness and alcohol on cognitive performance and self-assessment of performance. A total number of 46 subjects (mean age 26.5 years; 20 female) stayed for twelve consecutive days and nights in the AMSAN sleep laboratory in Cologne. According to the experimental protocol subjects were deprived of sleep totally and partially for two single nights during their stay. In addition, on one evening they consumed a moderate amount of alcohol. Every three hours during the time awake a computerized cognitive test-battery of pilot and air-traffic controller aptitudes was administered to the subjects including spatial orientation, perceptual speed, attention control and psychomotor precision. Additionally subjective levels of fatigue were measured periodically. Prior to and subsequent to each testing subjects were asked to assess their current level of performance for each of the aptitude areas. The accuracy of the self-assessments was analyzed in relation to the different cognitive areas under baseline conditions as well as under treatment conditions. The paper focusses on the comparison of prospective and retrospective accuracy of the self-assessments in relation to conditions of sleep restriction, alcohol consumption and subjective levels of fatigue.

Introduction: Both motivation and sleep deprivation affect cognitive performance. Especially during long-lasting studies with repeated cognitive performance tasks there is concern that subjects will lose motivation over time. Results may be confounded due to changes in motivation. Methods: In an ongoing study, 29 healthy volunteers performed 55 cognitive performance tasks at three-hourly intervals in a 12-day inpatient study. After two baseline nights with 8 h time in bed (TIB) the intervention group (N=20; mean age 26 ± 4 years, 9 females) underwent chronic sleep restriction for 5 nights (5 h TIB) with a following recovery night of 8 h TIB. The control group (N=9; mean age 25 ± 5 years, 3 females) had the opportunity to sleep 8 hours every night. Participants completed the Karolinska Sleepiness Scale (KSS) and a questionnaire about their motivation (from 1=very little/not motivated to 5=very motivated) at 6 p.m. on all days. Results: Wilcoxon signed-rank tests showed a significant decrease in motivation (p=.0439) and a significant increase in subjective sleepiness (p=.0184) from baseline (motivation: 2.8 ± 0.6 (SD), sleepiness: 3.2 ± 1.2) to the last day of chronic sleep restriction (motivation: 2.2 ± 0.5, sleepiness: 5.1 ± 1.8) for the experimental group. Motivation remained low after recovery sleep (2.2 ± 0.8; p=.0198). Sleepiness and motivation scores showed a significant Spearman correlation (r=-0.43, p