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Objective: To analyze patient-reported outcomes, cognitive function, and persistent symptoms in patients with neurologic post-acute sequelae of SARSCoV- 2 infection (Neuro-PASC) in Colombia. Methods: We recruited patients with laboratory-confirmed COVID-19 and PASC symptoms lasting more than 6 weeks at the CES University and CES Clinic (Medellín, Colombia). We included 50 post-hospitalization Neuro-PASC (PNP) and 50 non-hospitalized Neuro-PASC (NNP) patients. Long-COVID symptoms, cognitive (NIH Toolbox v2.1-Spanish for 18+), patient-reported (PROMIS) outcomes, and relevant medical history were evaluated. Statistical analyses were performed via generalized linear models. Results: Overall, brain fog (60%), myalgia (42%), and numbness or tingling (41%) were the most common neurological symptoms, while fatigue (74%), sleep problems (46%), and anxiety (44%) were the most common non-neurological symptoms. Compared to NNP, PNP patients showed a higher frequency of abnormal neurological exam findings (64% vs. 42%, p = 0.028). Both groups had impaired quality of life (QoL) in domains of cognition, fatigue, anxiety depression and sleep disturbance, and performed worse on processing speed and attention than a normative population. In addition, NNP patients performed worse on executive function than PNP patients (T-score 42.6 vs. 48.5, p = 0.012). PASC symptoms of anxiety and depression were associated with worse QoL and cognitive outcomes. Brain fog and fatigue remained persistent symptoms across all durations of Long COVID. Conclusion: Our findings highlight the high incidence and heterogeneity of the neurologic symptoms and impacts of Long COVID even more than 2 years from disease onset. Early detection, emotional support and targeted management of Neuro-PASC patients are warranted. [ABSTRACT FROM AUTHOR]

Introduction: ECG Derived Respiration (EDR) are a set of methods used for extracting the breathing rate from the Electrocardiogram (ECG). Recent studies revealed a tight connection between breathing rate and more specifically the breathing patterns during sleep and several related pathologies. Yet, while breathing rate and more specifically the breathing pattern is recognised as a vital sign it is less employed than Electroencephalography (EEG) and heart rate in sleep and polysomnography studies. Methods: This study utilised open-access data from the ISRUC sleep database to test a novel spectral-based EDR technique (scEDR). In contrast to previous approaches, the novel method emphasizes spectral continuity and not only the power of the different spectral peaks. scEDR is then compared against a more widely used spectral EDR method that selects the frequency with the highest power as the respiratory frequency (Max Power EDR). Results: scEDR yielded improved performance against the more widely used Max Power EDR in terms of accuracy across all sleep stages and the whole sleep. This study further explores the breathing rate across sleep stages, providing evidence in support of a putative sleep stage "REM0" which was previously proposed based on analysis of the Heart Rate Variability (HRV) but not yet widely discussed. Most importantly, this study observes that the frequency distribution of the heart rate during REM0 is closer to REM than other NREM periods even though most of REM0 was previously classified as NREM sleep by sleep experts following either the original or revised sleep staging criteria. Discussion: Based on the results of the analysis, this study proposes scEDR as a potential low-cost and non-invasive method for extracting the breathing rate using the heart rate during sleep with further studies required to validate its accuracy in awake subjects. In this study, the autonomic balance across different sleep stages, including REM0, was examined using HRV as a metric. The results suggest that sympathetic activity decreases as sleep progresses to NREM3 until it reaches a level similar to the awake state in REM through a transition from REM0. [ABSTRACT FROM AUTHOR]

Research on slow-wave sleep (SWS) began almost a century ago, not long after the discovery of electroencephalography. From maintaining homeostasis to memory function, the pivotal role of SWS in health has been established. The elucidation of its mechanisms and functions is directly related to the fundamental question of why people sleep. This comprehensive review first summarizes the basic science of SWS from anatomical and physiological aspects. It describes the fundamental mechanisms and functions of SWS, including hormonal regulation, developmental changes in SWS across the lifespan, and associations between SWS and optimal physical, psychological, and cognitive functions. Next, the relationship between SWS and physical and mental disorders, for which increasing knowledge has accumulated in recent years, is discussed from both research and clinical perspectives. Conditions such as memory impairment, sleep-disordered breathing, neurodevelopmental disorders, and various psychiatric disorders are of concern. The relationship between SWS and the glymphatic system, which is responsible for waste clearance in the brain, has also been explored, highlighting the potential neuroprotective role of SWS. Finally, we discuss the future direction of the field regarding whether interventions in SWS can improve health. We also address the problem of the inconsistent definitions of SWS, slow-wave activity, and slow oscillations. This review emphasizes the importance of discussing SWS from both macro- and microarchitectural perspectives and highlights its potential clinical and research impacts. By reviewing these aspects, we aim to contribute to a deeper understanding of SWS and the future development of this research field. [ABSTRACT FROM AUTHOR]

Objective: In the present study, we aimed to assess the cognition of post-COVID-19 condition (PCC) participants in relation to their subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI) and to analyse possible moderators of this effect, such as quality of life (European Quality of Life-5 Dimensions, EQ-5D), fatigue (Chadler Fatigue Questionnaire, CFQ), cognitive reserve (Cognitive Reserve Questionnaire, CRC), and subjective cognitive complaints (Memory Failures of Everyday Questionnaire, MFE-30). Methods: We included 373 individuals with PCC and 126 healthy controls (HCs) from the NAUTILUS Project (NCT05307549 and NCT05307575) who were assessed with a comprehensive neuropsychological battery and various questionnaires. Results: We found that PCC participants with poor sleep quality had a 4.3% greater risk of immediate verbal memory deficits than those with good sleep quality, as indicated by the greater odds ratio (OR) of 1.043 and confidence interval (CI) of 1.023-1.063. Additionally, their risk of immediate verbal memory disorders was multiplied by 2.4 when their EQ-5D score was low (OR 0.33; CI 0.145-0.748), and they had a lower risk of delayed visual memory deficits with a greater CRC (OR 0.963; CI 0.929-0.999). With respect to processing speed, PCC participants with poor sleep quality had a 6.7% greater risk of deficits as the MFE increased (OR 1.059; CI 1.024-1.096), and the risk of slowed processing speed tripled with a lower EQ-5D (OR 0.021; CI 0.003-0.141). Conclusion: These results indicate that poor subjective sleep quality is a potential trigger for cognitive deficits. Therapeutic strategies to maximize sleep quality could include reducing sleep disturbances and perhaps cognitive impairment in PCC individuals. [ABSTRACT FROM AUTHOR]

Due to worldwide demographic change, the number of older persons in the population is increasing. Aging is accompanied by changes of sleep structure, deposition of beta-amyloid (Aß) and tau proteins and vascular changes and can turn into mild cognitive impairment (MCI) as well as dementia. Sleep disorders are discussed both as a risk factor for and as a consequence of MCI/dementia. Cross-sectional and longitudinal population-based as well as case-control studies revealed sleep disorders, especially sleep-disorderded breathing (SDB) and excessive or insufficient sleep durations, as risk factors for all-cause MCI/dementia. Regarding different dementia types, SDB was especially associated with vascular dementia while insomnia/insufficient sleep was related to an increased risk of Alzheimer's disease (AD). Scarce and still inconsistent evidence suggests that therapy of sleep disorders, especially continuous positive airway pressure (CPAP) in SDB, can improve cognition in patients with sleep disorders with and without comorbid dementia and delay onset of MCI/dementia in patients with sleep disorders without previous cognitive impairment. Regarding potential pathomechanisms via which sleep disorders lead to MCI/dementia, disturbed sleep, chronic sleep deficit and SDB can impair glymphatic clearance of beta-amyloid (Aß) and tau which lead to amyloid deposition and tau aggregation resulting in changes of brain structures responsible for cognition. Orexins are discussed to modulate sleep and Aß pathology. Their diurnal fluctuation is suppressed by sleep fragmentation and the expression suppressed at the point of hippocampal atrophy, contributing to the progression of dementia. Additionally, sleep disorders can lead to an increased vascular risk profile and vascular changes such as inflammation, endothelial dysfunction and atherosclerosis which can foster neurodegenerative pathology. There is ample evidence indicating that changes of sleep structure in aging persons can lead to dementia and also evidence that therapy of sleep disorder can improve cognition. Therefore, sleep disorders should be identified and treated early. [ABSTRACT FROM AUTHOR]

Introduction: Autonomic nervous system (ANS) plays an important role in the exchange of metabolic information between organs and regulation on peripheral metabolism with obvious circadian rhythm in a healthy state. Sleep, a vital brain phenomenon, significantly affects both ANS and metabolic function. Objectives: This study investigated the relationships among sleep, ANS and metabolic function in type 2 diabetes mellitus (T2DM), to support the evaluation of ANS function through heart rate variability (HRV) metrics, and the determination of the correlated underlying autonomic pathways, and help optimize the early prevention, post-diagnosis and management of T2DM and its complications. Materials and methods: A total of 64 volunteered inpatients with T2DM took part in this study. 24-h electrocardiogram (ECG), clinical indicators of metabolic function, sleep quality and sleep staging results of T2DM patients were monitored. Results: The associations between sleep quality, 24-h/awake/sleep/sleep staging HRV and clinical indicators of metabolic function were analyzed. Significant correlations were found between sleep quality and metabolic function (|r| = 0.386 ± 0.062, p < 0.05); HRV derived ANS function showed strengthened correlations with metabolic function during sleep period (|r| = 0.474 ± 0.100, p < 0.05); HRV metrics during sleep stages coupled more tightly with clinical indicators of metabolic function [in unstable sleep: |r| = 0.453 ± 0.095, p < 0.05; in stable sleep: |r| = 0.463 ± 0.100, p < 0.05; in rapid eye movement (REM) sleep: |r| = 0.453 ± 0.082, p < 0.05], and showed significant associations with glycemic control in non-linear analysis [fasting blood glucose within 24 h of admission (admission FBG), |r| = 0.420 ± 0.064, p < 0.05; glycated hemoglobin (HbA1c), |r| = 0.417 ± 0.016, p < 0.05]. Conclusions: HRV metrics during sleep period play more distinct role than during awake period in investigating ANS dysfunction and metabolism in T2DM patients, and sleep rhythm based HRV analysis should perform better in ANS and metabolic function assessment, especially for glycemic control in non-linear analysis among T2DM patients. [ABSTRACT FROM AUTHOR]

Purpose: Current evidence of whether napping promotes or declines cognitive functions among older adults is contradictory. The aim of this study was to determine the association between nap duration and cognitive functions among Saudi older adults. Methods: Old adults (> 60 years) were identified from the Covid-19 vaccine center at Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia between May and August 2021. Face-to-face interviews were conducted by a geriatrician or family physicians. Data collected for each participant included sociodemographic, sleep patterns, health status and cognitive functions. St. Louis University mental status (SLUMS) was used to assess the cognitive functions. A multi-Linear regression model was used to determine the association between cognitive functions and nap duration. Results: Two-hundred participants (58 females) aged 66 ± 5 years were recruited. Participants were categorized according to their nap duration into non-nappers (0 min), short nappers (> 0- ≤ 30 min), moderate nappers (> 30–≤ 90 min), and extended nappers (> 90 min). The mean duration of the nap was 49.1 ± 58.4 min. The mean SLUMS score was 24.1 ± 4.7 units. Using the multi-linear regression model, the mean total SLUMS score for extended nappers was, on average, significantly lower than non-nappers [−2.16 units; 95% CI (−3.66, −0.66), p = < 0.01] after controlling for the covariates (age, sex, education level, sleep hours, diabetes mellitus, hypertension, pain). Conclusions: Extended napping was associated with deterioration in cognitive function among Saudi older adults. [ABSTRACT FROM AUTHOR]

Late-onset Alzheimer's disease (AD) is associated with sleep-related phenotypes (SRPs). The fact that whether they share a common genetic etiology remains largely unknown. We explored the shared genetics and causality between AD and SRPs by using high-definition likelihood (HDL), cross-phenotype association study (CPASSOC), transcriptome-wide association study (TWAS), and bidirectional Mendelian randomization (MR) in summary-level data for AD (N = 455,258) and summary-level data for seven SRPs (sample size ranges from 359,916 to 1,331,010). AD shared a strong genetic basis with insomnia (r g = 0.20; p = 9.70 × 10–5), snoring (r g = 0.13; p = 2.45 × 10–3), and sleep duration (r g = −0.11; p = 1.18 × 10–3). The CPASSOC identifies 31 independent loci shared between AD and SRPs, including four novel shared loci. Functional analysis and the TWAS showed shared genes were enriched in liver, brain, breast, and heart tissues and highlighted the regulatory roles of immunological disorders, very-low-density lipoprotein particle clearance, triglyceride-rich lipoprotein particle clearance, chylomicron remnant clearance, and positive regulation of T-cell–mediated cytotoxicity pathways. Protein–protein interaction analysis identified three potential drug target genes (APOE , MARK4 , and HLA-DRA) that interacted with known FDA-approved drug target genes. The CPASSOC and TWAS demonstrated three regions 11p11.2, 6p22.3, and 16p11.2 may account for the shared basis between AD and sleep duration or snoring. MR showed insomnia had a causal effect on AD (ORIVW = 1.02, P IVW = 6.7 × 10–6), and multivariate MR suggested a potential role of sleep duration and major depression in this association. Our findings provide strong evidence of shared genetics and causation between AD and sleep abnormalities and advance our understanding of the genetic overlap between them. Identifying shared drug targets and molecular pathways can be beneficial for treating AD and sleep disorders more efficiently. [ABSTRACT FROM AUTHOR]

Objective: The relationship between sleep problems and walking speed has been less explored. The present cross-sectional study was to investigate the association between sleep quality and sleep duration and gait speed in Chinese adults. Methods: A total of 13,367 participants were recruited in this cross-sectional study, retrieving the data from the Global Aging and Adult Health Survey (SAGE). Gait speed was measured using the 4-m walking test. Age, sex, education years, smoking status, alcohol consumption, physical activity, chronic disease, sleep problems were self-reported by participants. To explore the association between sleep problems and gait speed, multivariate linear regression models were employed. Results: In the adjusted model, poor sleep quality and longer sleep duration were significantly associated with slower normal walking speed in Chinese adults (p < 0.001). Moreover, there were negatively significant associations between normal gait speed and sleep quality in male adults (p < 0.01). Conclusion: The findings suggest that slower normal walking speed was associated with poor sleep quality and longer sleep duration (>8 h) in Chinese male adults. [ABSTRACT FROM AUTHOR]

Mild Cognitive Impairment (MCI) is an early stage of dementia, which may lead to Alzheimer's disease (AD) in older adults. Therefore, early detection of MCI and implementation of treatment and intervention can effectively slow down or even inhibit the progression of the disease, thus minimizing the risk of AD. Currently, we know that published work relies on an analysis of awake EEG recordings. However, recent studies have suggested that changes in the structure of sleep may lead to cognitive decline. In this work, we propose a sleep EEG-based method for MCI detection, extracting specific features of sleep to characterize neuroregulatory deficit emergent with MCI. This study analyzed the EEGs of 40 subjects (20 MCI, 20 HC) with the developed algorithm. We extracted sleep slow waves and spindles features, combined with spectral and complexity features from sleep EEG, and used the SVM classifier and GRU network to identify MCI. In addition, the classification results of different feature sets (including with sleep features from sleep EEG and without sleep features from awake EEG) and different classification methods were evaluated. Finally, the MCI classification accuracy of the GRU network based on features extracted from sleep EEG was the highest, reaching 93.46%. Experimental results show that compared with the awake EEG, sleep EEG can provide more useful information to distinguish between MCI and HC. This method can not only improve the classification performance but also facilitate the early intervention of AD. [ABSTRACT FROM AUTHOR]

Background: Adolescents with a late chronotype are at greater risk for mood disorders, risk-taking behaviors, school absenteeism, and lower academic achievement. As there are multiple causes for late chronotype, the field lacks studies on the relationship between mood, circadian phase, and phase angle of entrainment in late chronotype adolescents. Three objectives guide this explorative study: (1) to describe sleep, circadian phase, and phase angle of entrainment in late chronotype adolescents, (2) to explore how different levels of lateness are associated with sleep quality, sleep propensity, and mood, and (3) to investigate the influence of circadian phase on bedtime choice and sleep duration. Methods: Baseline data from 19 male adolescents (M = 16.4 ± 1.0 yrs), who were part of a larger intervention trial, were analyzed. Chronotype was measured with the Munich Chronotype Questionnaire, circadian timing via dim light melatonin onset (DLMO), and sleep habits with a 7-day sleep log. Further questionnaires assessed daytime sleepiness, sleep quality, and mood. Evening sleepiness and sustained attention were used as a proxy for evening sleep propensity. Results: On school nights, sleep duration averaged 7.78 h (±1.65), and 9.00 h (±1.42) on weekend nights. Mean DLMO was observed at 23.13 h (± 1.65), with a weekend phase angle of entrainment of 2.48 h. Regression fittings revealed a tendency for shorter phase angles with delayed DLMOs. Further analysis with chronotype subgroups revealed that this was only true for light and moderate late types, whereas extreme late types showed wide phase angles. Even though daytime sleepiness and sleep duration did not differ between subgroups, mood and sleep quality declined as lateness increased. Extreme late chronotypes experienced higher evening sleepiness, while slight late chronotypes showed higher evening attention. Chronotype but not DLMO predicted bedtime on school- and particularly weekend-nights. Conclusions: Our findings suggest that with increasing lateness, the likelihood of experiencing poor sleep quality and mood disorders increases. As DLMO did not predict bedtime, our data indicate that the factors contributing to a late chronotype are versatile and complex, particularly for extreme late types. Further studies involving a larger and gender-balanced sample are needed to confirm findings. [ABSTRACT FROM AUTHOR]

The aim of the study is to determine the association between Behavioral Lifestyles (regular physical activity, healthy diet, sleeping, and weight control) and longevity in the elderly. A search strategy was conducted in the PsycInfo, Medline, PubMed, Web of Science (WoS), and Scopus databases. The primary outcome was mortality/survival. Four variables (mean of participant's age at the baseline of the study, follow-up years of the study, gender, and year of publication) were analyzed to evaluate the role of potential moderators. Ninety-three articles, totaling more than 2,800,000 people, were included in the meta-analysis. We found that the lifestyles analyzed predict greater survival. Specifically, doing regular physical activity, engaging in leisure activities, sleeping 7–8 h a day, and staying outside the BMI ranges considered as underweight or obesity are habits that each separately has a greater probability associated with survival after a period of several years. [ABSTRACT FROM AUTHOR]

Background: Sleep duration is linked to cognitive function, but whether short or prolonged sleep duration results from impaired cognition or vice versa has been controversial in previous studies. We aimed to investigate the bidirectional association between sleep duration and cognitive function in older Chinese participants. Methods: Data were obtained from a nationally representative study conducted in China. A total of 7984 participants aged 45 years or older were assessed at baseline between June 2011 and March 2012 (Wave 1), 2013 (Wave 2), 2015 (Wave 3), and 2018 (Wave 4). Nocturnal sleep duration was evaluated using interviews. Cognitive function was examined via assessments of global cognition, including episodic memory, visuospatial construction, calculation, orientation and attention capacity. Latent growth models and cross-lagged models were used to assess the bidirectional association between sleep duration and cognitive function. Results: Among the 7,984 participants who were followed in the four waves of the study, the baseline mean (SD) age was 64.7 (8.4) years, 3862 (48.4%) were male, and 6453 (80.7%) lived in rural areas. Latent growth models showed that both sleep duration and global cognition worsened over time. Cross-lagged models indicated that short or long sleep duration in the previous wave was associated with lower global cognition in the subsequent wave (standardized β = −0.066; 95% CI: −0.073, −0.059; P < 0.001; Wave 1 to 2) and that lower global cognition in the previous wave was associated with short or long sleep duration in the subsequent wave (standardized β = −0.106; 95% CI: −0.116, −0.096; P < 0.001; Wave 1 to 2). Conclusion: There was a bidirectional association between sleep duration and cognitive function, with lower cognitive function having a stronger association with long or short sleep duration than the reverse relationship. Global cognition was likely the major driver in these reciprocal associations. [ABSTRACT FROM AUTHOR]

Current approaches to quantify and diagnose sleep disorders and circadian rhythm disruption are imprecise, laborious, and often do not relate well to key clinical and health outcomes. Newer emerging approaches that aim to overcome the practical and technical constraints of current sleep metrics have considerable potential to better explain sleep disorder pathophysiology and thus to more precisely align diagnostic, treatment and management approaches to underlying pathology. These include more fine-grained and continuous EEG signal feature detection and novel oxygenation metrics to better encapsulate hypoxia duration, frequency, and magnitude readily possible via more advanced data acquisition and scoring algorithm approaches. Recent technological advances may also soon facilitate simple assessment of circadian rhythm physiology at home to enable sleep disorder diagnostics even for "non-circadian rhythm" sleep disorders, such as chronic insomnia and sleep apnea, which in many cases also include a circadian disruption component. Bringing these novel approaches into the clinic and the home settings should be a priority for the field. Modern sleep tracking technology can also further facilitate the transition of sleep diagnostics from the laboratory to the home, where environmental factors such as noise and light could usefully inform clinical decision-making. The "endpoint" of these new and emerging assessments will be better targeted therapies that directly address underlying sleep disorder pathophysiology via an individualized, precision medicine approach. This review outlines the current state-of-the-art in sleep and circadian monitoring and diagnostics and covers several new and emerging approaches to better define sleep disruption and its consequences. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effects of placebo (PLA), 20 min nap opportunity (N20), 5mg·kg−1 of caffeine (CAF), and their combination (CAF+N20) on sleepiness, mood and reaction-time after partial sleep deprivation (PSD; 04h30 of time in bed; study 1) or after normal sleep night (NSN; 08h30 of time in bed; study 2). Methods: Twenty-three highly trained athletes (study 1 ; 9 and study 2 ; 14) performed four test sessions (PLA, CAF, N20 and CAF+N20) in double-blind, counterbalanced and randomized order. Simple (SRT) and two-choice (2CRT) reaction time, subjective sleepiness (ESS) and mood state (POMS) were assessed twice, pre- and post-intervention. Results: SRT was lower (i.e., better performance) during CAF condition after PSD (pre: 336 ± 15 ms vs. post: 312 ± 9 ms; p < 0.001; d = 2.07; Δ% = 7.26) and NSN (pre: 350 ± 39 ms vs. post: 323 ± 32 ms; p < 0.001; d = 0.72; Δ% = 7.71) compared to pre-intervention. N20 decreased 2CRT after PSD (pre: 411 ± 13 ms vs. post: 366 ± 20 ms; p < 0.001; d = 2.89; Δ% = 10.81) and NSN (pre: 418 ± 29 ms vs. post: 375 ± 40 ms; p < 0.001; d = 1.23; Δ% = 10.23). Similarly, 2CRT was shorter during CAF+N20 sessions after PSD (pre: 406 ± 26 ms vs. post: 357 ± 17 ms; p < 0.001; d = 2.17; Δ% = 12.02) and after NSN (pre: 386 ± 33 ms vs. post: 352 ± 30 ms; p < 0.001; d = 1.09; Δ% = 8.68). After PSD, POMS score decreased after CAF (p < 0.001; d = 2.38; Δ% = 66.97) and CAF+N20 (p < 0.001; d = 1.68; Δ% = 46.68). However, after NSN, only N20 reduced POMS (p < 0.001; d = 1.05; Δ% = 78.65) and ESS (p < 0.01; d = 0.71; Δ% = 19.11). Conclusion: After PSD, all interventions reduced sleepiness and only CAF enhanced mood with or without napping. However, only N20 enhanced mood and reduced sleepiness after NSN. Caffeine ingestion enhanced SRT performance regardless of sleep deprivation. N20, with or without caffeine ingestion, enhanced 2CRT independently of sleep deprivation. This suggests a different mode of action of napping and caffeine on sleepiness, mood and reaction time. [ABSTRACT FROM AUTHOR]

Fatigue poses an important safety risk to civil and military aviation. In addition to decreasing performance in-flight (chronic) fatigue has negative long-term health effects. Possible causes of fatigue include sleep loss, extended time awake, circadian phase irregularities and work load. Despite regulations limiting flight time and enabling optimal rostering, fatigue cannot be prevented completely. Especially in military operations, where limits may be extended due to operational necessities, it is impossible to rely solely on regulations to prevent fatigue. Fatigue management, consisting of preventive strategies and operational countermeasures, such as pre-flight naps and pharmaceuticals that either promote adequate sleep (hypnotics or chronobiotics) or enhance performance (stimulants), may be required to mitigate fatigue in challenging (military) aviation operations. This review describes the pathophysiology, epidemiology and effects of fatigue and its impact on aviation, as well as several aspects of fatigue management and recommendations for future research in this field. [ABSTRACT FROM AUTHOR]

Background: Growing evidence has suggested a link between poor sleep quality and increased risk of dementia. However, little is known about the association between sleep timing, an important behavior marker of circadian rhythms, and dementia risk in older adults, and whether this is independent of sleep duration or quality. Methods: We included data from 1,051 community-dwelling older men and women (aged≥ 60y) without dementia from the Shanghai Aging Study. At baseline, participants reported sleep timing, duration, and quality using the Chinese version of the Pittsburgh Sleep Quality Index (CPSQI). Dementia diagnosis over the following 7.3 years was determined by neurologists using DSM-IV criteria. We used Cox proportional hazards models to examine the association between bedtime (before 9 p.m., after 11 p.m. vs. 9–11 p.m.), rise time (before 6 a.m., after 8 a.m. vs. 6–8 a.m.), and risk of dementia. Results: A total of 238 (22.8%), 675 (64.5%), and 133 (12.7%) participants reported going to bed before 9 p.m., between 9 and 11 p.m., and after 11 p.m., respectively, while 272 (26%), 626 (59.9%), and 148 (14.2%) reported getting up before 6 a.m., between 6 and 8 a.m., and after 8 a.m., respectively. Participants who reported going to bed earlier had a lower education level, were less likely to be smokers, more likely to have hypertension or diabetes, and had longer sleep duration but poorer sleep quality compared to those who reported a later bedtime. We found 47 incidents of dementia among 584 participants followed up over an average of 7.3 years. After adjustment for demographics, education, income, body mass index, depressive symptoms, smoking, alcohol use, physical activity, comorbidities, APOE4 genotype, and baseline MMSE, those with a bedtime of before 9 p.m. were two times more likely to develop dementia [hazard ratio (HR)=2.16 (95%CI: 1.06–4.40)], compared to those going to bed between 9 and 11 p.m. Later bedtime (i.e., after 11 p.m.) showed the opposite but had a non-significant association with dementia risk (HR=0.15, 95%CI: 0.02–1.29). We did not find an association for rise time and risk of dementia. Conclusion: Earlier sleep timing in older adults without dementia was associated with an increased risk of dementia. Future studies should examine the underlying mechanisms of this association and explore the usefulness of sleep timing as a preclinical marker for dementia. [ABSTRACT FROM AUTHOR]

Both short (<7 h per night) and long (≥9 h per night) sleep durations are related to atrial fibrillation (AF) and heart failure (HF), but their causality has not been confirmed. We applied Mendelian randomization (MR) approaches to estimate the causal association between genetically determined sleep duration and the risk of AF and HF. We performed two-sample MR analysis to obtain the effect of sleep duration on AF and HF. Instrumental variables were constructed using genetic variants known to be associated with continuous sleep duration, short sleep duration, and long sleep duration. MR estimates of the effect of sleep duration on AF and HF were derived based on two large meta-analyses of genome-wide association studies. The pooled MR estimate demonstrated a significant protective effect of continuous sleep duration on HF [odds ratio (OR) = 0.765, 95% confidence interval (CI) = 0.675–0.867; P = 2.64 × 10–5] and a suggestive inverse association of continuous sleep duration with AF (OR = 0.893, 95% CI = 0.804–0.991; P = 0.034). In addition, the results showed a suggestive detrimental effect of short sleep duration on the risk of AF (OR = 1.108, 95% CI = 1.017–1.207; P = 0.019) and HF (OR = 1.136, 95% CI = 1.025–1.258; P = 0.015). Conversely, there is no significant evidence for the causal protective effect of long sleep duration on AF (OR = 0.956, P = 0.410) and HF (OR = 0.921, P = 0.202). This MR study indicated that genetically determined continuous sleep duration has a significant protective effect on HF and a suggestive inverse association with AF. Short sleep duration is positively associated with the risk of AF and HF. Nevertheless, there is no significant evidence for the causal protective effect of long sleep duration on AF and HF. Larger intervention studies are required to confirm the effectiveness of improving sleep on reducing the incidence of AF and HF. [ABSTRACT FROM AUTHOR]

Purpose: The COVID-19 pandemic caused a massive healthcare crisis. To investigate what makes healthcare system resilient and physicians better at coping during a crisis situation, our study investigated the role risk exposure, such as working at COVID-19 entry points, sleep, and perceived work safety played in reducing negative psychological functioning at work, as well as their effects on adverse and potentially fatal incidences of compromised safety and medical errors. Methods: Our study included a representative sample of 1,189 physicians, from all 12 Slovenian regions and all medical occupations, as registered by the Medical Chamber of Slovenia. For the purposes of this study, a Questionnaire of Sleep and Psychological Functioning at Work was developed in the form of an online retrospective self-report. Additionally, our study included items assessing physicians perceived work safety and frequency of negative outcomes (compromised safety and medical errors) during the first month of the Covid-19 epidemic. Results: Physicians working at COVID-19 entry points were more likely to experience night awakening, slept less than 5 h per night, experience nightmares, and had lower levels of psychological functioning in comparison to other physicians. Both hypothesized models showed adequate fit. A higher score on the sleep scale (sleep quantity, sleep quality, and shorter sleep latency) has been shown to predict lower levels of negative psychological functioning at work and, indirectly, reduced incidences of compromised safety and medical errors. Contrary to our expectations, no significant direct effect of sleep on compromised safety and medical errors was found. When perceived work safety was added into the model, the model showed improved fit, with perceived work safety predicting better sleep, less negative psychological functioning at work, and less compromised safety. Conclusion: Sleep and safety both play an important role in reducing negative psychological functioning at work and, by doing so, decreasing the negative and potentially fatal incidents during the pandemic, such as compromised safety and medical errors. Further, research is needed to see how medical guidelines can be updated to ensure physicians sleep and that their safety is protected. [ABSTRACT FROM AUTHOR]

Disruptions of sleep and circadian rhythms are among the most debilitating symptoms in patients with neurodegenerative diseases. Their underlying pathophysiology is multilayered and multifactorial. Recent evidence suggests that sleep and circadian disturbances may influence the neurodegenerative processes as well as be their consequence. In this perspective, we provide an update of the current understanding of sleep and circadian dysregulation in Alzheimer's, Parkinson's, and Huntington's diseases. [ABSTRACT FROM AUTHOR]

Sleep is crucial for optimal well-being, and sex differences in sleep quality have significant implications for women's health. We review the current literature on sex differences in sleep, such as differences in objective and subjective sleep measures and their relationship with aging. We then discuss the convincing evidence for the role of ovarian hormones in regulating female sleep, and survey how these hormones act on a multitude of brain regions and neurochemicals to impact sleep. Lastly, we identify several important areas in need of future research to narrow the knowledge gap and improve the health of women and other understudied populations. [ABSTRACT FROM AUTHOR]

Study objectives: To investigate the extent to which sleep quality associated with plasma Aβ levels in amnestic mild cognitive impairment (aMCI) elderly. Methods: A total of 172 cognitively normal (NC) elderly and 133 aMCI elderly were included in this study. For the evaluation of sleep quality, the Pittsburgh Sleep Quality Index (PSQI) was used. Levels of plasma Aβ were determined by the sandwich enzyme-linked immunosorbent assay technique. Multivariable linear regression analysis was applied to evaluate associations between sleep quality and plasma Aβ levels after adjusting potential confounders. Results: Compared to NC subjects, participants with aMCI had a higher global PSQI score (8.72 ± 3.87 vs. 7.10 ± 3.07, p < 0.001). The global PSQI score was positively associated with plasma Aβ42 level in the aMCI group (β = 0.063, 95% CI 0.001–0.125, and p = 0.049) but not in the NC group (p > 0.05). Additionally, a higher global PSQI score was associated with a higher plasma Aβ42/Aβ40 ratio in both NC (β = 0.010, 95% CI 0.003–0.016, and p = 0.003) and aMCI groups (β = 0.012, 95% CI 0.005–0.018, and p < 0.001). The association between global PSQI score and plasma Aβ42/Aβ40 ratio was stronger in individuals with aMCI relative to the NC subjects (β = 0.076 vs. 0.030, p for interaction = 0.023). Conclusion: Poor sleep quality was associated with plasma Aβ42 and Aβ42/Aβ40 ratio, with a stronger effect among individuals with aMCI. A better understanding of the role of sleep in plasma Aβ levels in aMCI patients could lead to effective sleep-based intervention against the risk of Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Circadian rhythm misalignment has a deleterious impact on the brain and the body. In rats, exposure to a 21-hour day length impairs hippocampal dependent memory. Sleep, and particularly K-complexes and sleep spindles in the cortex, have been hypothesized to be involved in memory consolidation. Altered K-complexes, sleep spindles, or interaction between the cortex and hippocampus could be a mechanism for the memory consolidation failure but has yet to be assessed in any circadian misalignment paradigm. In the current study, continuous local field potential recordings from five rats were used to assess the changes in aspects of behavior and sleep, including wheel running activity, quiet wakefulness, motionless sleep, slow wave sleep, REM sleep, K-complexes and sleep spindles, in rats exposed to six consecutive days of a T21 light-dark cycle (L9:D12). Except for a temporal redistribution of sleep and activity during the T21, there were no changes in period, or total amount for any aspect of sleep or activity. These data suggest that the memory impairment elicited from 6 days of T21 exposure is likely not due to changes in sleep architecture. It remains possible that hippocampal plasticity is affected by experiencing light when subjective circadian phase is calling for dark. However, if there is a reduction in hippocampal plasticity, changes in sleep appear not to be driving this effect. [ABSTRACT FROM AUTHOR]

Andean highlanders are challenged by chronic hypoxia and many exhibit elevated hematocrit (Hct) and blunted ventilation compared to other high-altitude populations. While many Andeans develop Chronic Mountain Sickness (CMS) and excessive erythrocytosis, Hct varies markedly within Andean men and women and may be driven by individual differences in ventilatory control and/or sleep events which exacerbate hypoxemia. To test this hypothesis, we quantified relationships between resting ventilation and ventilatory chemoreflexes, sleep desaturation, breathing disturbance, and Hct in Andean men and women. Ventilatory measures were made in 109 individuals (n = 63 men; n = 46 women), and sleep measures in 45 of these participants (n = 22 men; n = 23 women). In both men and women, high Hct was associated with low daytime SpO2 (p < 0.001 and p < 0.002, respectively) and decreased sleep SpO2 (mean, nadir, and time <80%; all p < 0.02). In men, high Hct was also associated with increased end-tidal PCO2 (p < 0.009). While ventilatory responses to hypoxia and hypercapnia did not predict Hct, decreased hypoxic ventilatory responses were associated with lower daytime SpO2 in men (p < 0.01) and women (p < 0.009) and with lower nadir sleep SpO2 in women (p < 0.02). Decreased ventilatory responses to CO2 were associated with more time below 80% SpO2 during sleep in men (p < 0.05). The obstructive apnea index and apnea-hypopnea index also predicted Hct and CMS scores in men after accounting for age, BMI, and SpO2 during sleep. Finally, heart rate response to hypoxia was lower in men with higher Hct (p < 0.0001). These data support the idea that hypoventilation and decreased ventilatory sensitivity to hypoxia are associated with decreased day time and nighttime SpO2 levels that may exacerbate the stimulus for erythropoiesis in Andean men and women. However, interventional and longitudinal studies are required to establish the causal relationships between these associations. [ABSTRACT FROM AUTHOR]

Objective : The aim of this study was to analyze quantitative sleep changes and their implication on subjective cognitive decline (SCD). Objective sleep patterns were investigated by an actigraph and recorded at the baseline and 2-year after in order to examine specific sleep alterations in SCD. Background : Sleep disorders are very common among average elderly adults and an altered sleep pattern is known to be a risk factor for future development of mild cognitive impairment (MCI) and dementia. Recent studies have shown how sleep is objectively altered in average senior adults with SCD, without any other significant change in cognition and behavior or brain structure. Considering that both SCD and disrupted sleep are risk factors for future MCI and dementia, with sleep only as a modifiable risk factor, further research is required to deeply investigate the interaction between sleep and SCD. Methods : Among 70 community-dwelling elderly individuals who had been enrolled at baseline, 35 (64.6 ± 5.6 years, 15 M/20 F) underwent a complete neuropsychological battery and 1-week wrist actigraphy recording 2 years later during the follow-up stage. Individuals were divided into two groups according to their SCD Questionnaire (SCD-Q) score. Sleep hours, sleep efficiency and onset latency, napping and time awake after sleep onset (WASO) were collected. All individuals underwent structural magnetic resonance imaging (MRI) examination to exclude brain disorders. Data collection was performed at baseline and after 2 years at the follow-up phase. Results : A significantly different night sleep time between the two groups was observed: SCD showed a lower total sleep time (TST) than non-SCD subjects. Moreover, a total time spent in bed (TIB) was significantly lower in SCD subjects over 2 years of observation. Conclusions : Objective changes over time of the sleep pattern, specifically TIB and TST, are present in SCD individuals. The results of the study show that sleep alterations are common in SCD and underline the clinical importance of screening in order to assess sleep alterations as well as improve sleep in average adults with SCD complaints. [ABSTRACT FROM AUTHOR]

Sedentary behavior (SB) has emerged as an independent public-health risk and may contribute to the lower bone mineral density (BMD) in old (>60 years of age) than young adults. The purpose of this study was to quantify SB and habitual physical behavior (PB) in community-dwelling older adults and how this correlates with BMD. In 112 relatively healthy and independent-living individuals aged 72.5 ± 6.4 years, BMD, PB and SB were determined using dual energy X-ray absorptiometry and 7-day three-dimensional accelerometry, respectively. In men, only healthy and osteopenic BMDs were found, whereas in women, osteoporotic BMD classifications also occurred. Our sample spent ∼61%, 7%, 12% and 19% of daily waking hours in SB, standing, LIPA [light intensity physical activity (PA)] and MVPA (medium-to-vigorous intensity PA), respectively. In men, after accounting for covariates (BMI, total fat, android:gynoid ratio), sleeping (hours/day), number of breaks in SB, number of SB ≥ 5 min, number of PA bouts, total duration of PA bouts (min), mean PA bouts duration (min), LIPA (%PA bout time) and MVPA (%PA bout time) were all predictors of BMD. In women, after accounting for covariates (age, BMI, total fat, android:gynoid ratio), SB (hours/day), SB (% waking hours), LIPA (hours/day), LIPA (% waking hours), MVPA (% waking hours) and number of short SB (i.e., <5 min), total time spent in PA (min) significantly correlated with BMD. In conclusion, the PB predictors of bone health in older persons include: night time sleeping duration, number of short bouts of SB, number and duration of bouts of PA relative to total waking hours. While radar graphs of PB patterns for healthy, osteopenic, osteoporotic individuals highlighted significant differences in PB between them, they were not consistent with the expectations from the Mechanostat Theory: i.e., more loading leads to better bone. Rather, our results suggest that a balance of activities must be maintained across the PB spectrum, where certain PB parameters are especially impactful in each sex, supporting the recently coined multifactorial-based variations in the Mechanostat threshold. [ABSTRACT FROM AUTHOR]

Objectives: The aims of the current study are to (1) report the frequency of specific sleep disturbance symptoms in Mild Cognitive Impairment (MCI) and cognitive healthy older persons; (2) examine whether overall poor sleep and specific sleep disturbance symptoms are more common in persons with MCI compared to cognitive healthy older controls and; (3) examine the association between sleep disturbances and performance in general and specific cognitive domains in persons with MCI and separately in cognitive healthy older persons. Methods: Data were collected at the Fondazione Ospedale San Camillo Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Venice, Italy as part of the European VPH-DARE@IT project. We included 69 persons with MCI (mean age 75.7; SD = 7.7) and 72 sex-matched cognitively healthy controls (mean age 71.8; SD = 7.0). Participants underwent extensive neuropsychological assessment and evaluation of subjective sleep performance with the Sleep Continuity in Alzheimer's Disease Scale(SCADS). Results: A fifth of MCI patients (21.7%, n = 15) had poor sleep compared to 15.3% (n = 11) of cognitively healthy controls. MCI patients had a 3.2 higher odds of having poor sleep compared to cognitively healthy controls after adjustment for age, education, sex, and general cognitive functioning (Odds Ratio (OR) = 3.2; 95% Confidence Interval (CI) = 1.1–9.2). Persons who reported waking up twice or more during the night had higher odds of being MCI compared to those who never wake or wake only once (OR = 2.6; 95% CI = 1.1–6.1). In MCI patients, poor sleep was associated with better general cognitive functioning and short-term working memory, whereas in cognitive healthy older persons poor sleep was associated with impairment in episodic memory performance and executive functioning. Discussion: Our results confirm previous studies showing that sleep disturbances are common in MCI, and this may be due to an ongoing neurodegenerative process rather than a symptom of cognitive impairment. Future research with objective sleep measurements are needed in MCI as well as interventions to improve sleep with the aim of preventing cognitive decline. [ABSTRACT FROM AUTHOR]

Promoting a healthy sleep is a big challenge and becomes a strategic priority in public health, due to the severe consequences on children’s development and risk to psychiatric diseases. Interventions that promote healthy sleep, such as those that focus on the dissemination of behavioral and environmental recommendations of sleep hygiene with children, are presented as an alternative. Serious game design offers wide-reaching domains in health applications and is increasing in popularity, particularly with children and teens because of it’s potential to engage and motivate players differently from other interventions. This study aims to evaluate effects of serious game on sleep hygiene recommendations “Perfect Bedroom: learn to sleep well,” on sleep habits and sleep parameters of healthy children. This is an experimental, prospective and quantitative study. We will randomize children in experimental (n = 88) and no intervention groups (n = 88). The experiment has four stages (pre-intervention, intervention, post-intervention, and follow-up), which will count with participation of children and their parents/guardians. In the evaluation stages, the guardians will answer questionnaires and scales to assess sociodemographic and health data, sleep habits and sleep pattern of their child. The children themselves will answer the following: a scale to assess sleepiness levels, a questionnaire to evaluate the serious game and the game itself, will characterize their bedroom and the activities they perform before sleep, with strategies developed by researches. Intervention with experimental group conducted with the serious game “Perfect Bedroom” will happen twice a week, for 3 weeks in a row, resulting in six sessions of 50 min each. Inferential analysis will be conducted for comparisons between groups and intragroups to measure effect of intervention in primary outcomes (sleep habits) and secondary outcomes (sleep parameters). We expect that the intervention with this game can provide valuable evidence to a new approach in promoting healthy sleep habits, with applications in clinical, educational, and familiar settings, which could diminish future health issues and risk at psychiatric diseases, decreasing the social burden of treatments for these conditions in children. [ABSTRACT FROM AUTHOR]

Objective: Previous research indicates that pain treatment may improve sleep among nursing home patients. We aimed to investigate the long-term effect of pain treatment on 24-h sleep patterns in patients with comorbid depression and dementia. Design: A 13-week, multicenter, parallel-group, double-blind, placebo-controlled randomized clinical trial conducted between August 2014 and September 2016. Setting: Long-term patients from 47 nursing homes in Norway. Participants: We included 106 patients with comorbid dementia and depression according to the Mini Mental Status Examination (MMSE) and the Cornell Scale for Depression in Dementia (CSDD). Intervention: Patients who were not using analgesics were randomized to receive either paracetamol (3 g/day) or placebo tablets. Those who already received pain treatment were randomized to buprenorphine transdermal system (maximum 10 μg/h/7 days) or placebo transdermal patches. Measurements: Sleep was assessed continuously for 7 days by actigraphy, at baseline and in week 13. Total sleep time (TST), sleep efficiency (SE), sleep onset latency (SOL), wake after sleep onset (WASO), early morning awakening (EMA), and number of wake bouts (NoW) were evaluated. In addition, daytime total sleep time (DTS) was estimated. Pain was assessed with Mobilization-Observation-Behavior-Intensity-Dementia-2 Pain Scale (MOBID-2). Results: The linear mixed model analyses for TST, SE, SOL, WASO, EMA, NoW and DTS showed no statistically significant differences between patients who received active pain treatment and those who received placebo. Post hoc subgroup analyses showed that there were no statistically significant differences between active treatment and placebo from baseline to week 13 in patients who were in pain (MOBID-2 ≥ 3) at baseline, or in patients who had poor sleep (defined as SE < 85%) at baseline. Patients who received active buprenorphine showed an increase in TST and SE compared to those who received active paracetamol. Conclusion: The main analyses showed that long-term pain treatment did not improve sleep as measured with actigraphy. Compared to paracetamol, TST and SE increased among patients who received buprenorphine. This could indicate that some patients had beneficial effects from the most potent pain treatment. However, based on the present findings, long-term pain treatment is not recommended as a strategy to improve sleep. Clinical Trial https://clinicaltrials.gov/ct2/show/NCT02267057. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is a common sleep breathing disorder associated with an increased risk of cardiovascular and cerebrovascular diseases and mortality. Although OSA is fairly heritable (~40%), there have been only few studies looking into the genetics of OSA. In the present study, we aimed to identify genetic variants associated with symptoms of sleep apnea by performing a whole-exome sequence meta-analysis of symptoms of sleep apnea in 1,475 individuals of European descent. We identified 17 rare genetic variants with at least suggestive evidence of significance. Replication in an independent dataset confirmed the association of a rare genetic variant (rs2229918; minor allele frequency = 0.3%) with symptoms of sleep apnea (p-valuemeta = 6.98 × 10-9, βmeta = 0.99). Rs2229918 overlaps with the 3' untranslated regions of ERCC1 and CD3EAP genes on chromosome 19q13. Both genes are expressed in tissues in the neck area, such as the tongue, muscles, cartilage and the trachea. Further, CD3EAP is localized in the nucleus andmitochondria and involved in the tumor necrosis factor-alpha/nuclear factor kappa B signaling pathway. Our results and biological functions of CD3EAP/ERCC1 genes suggest that the 19q13 locus is interesting for further OSA research. [ABSTRACT FROM AUTHOR]

Objective: To identify self-reported sleep-wake disturbances that increase the risk of cognitive decline over 1-year follow-up in frail participants. Background: Risk factors for cognitive impairment need to be better identified especially at earliest stages of the pathogenesis. Sleep-wake disturbances may be critical factors to consider and were thus being assessed in this at-risk population for cognitive decline. Methods: Frail elderly participants aged ≥70 years were selected from a subsample of the Multi-domain Alzheimer Preventive Trial (MAPT) for a sleep assessment (MAPT-sleep study) at 18-month follow-up (M18). Sleep-wake disturbances were evaluated using a clinical interview (duration of daytime and nighttime sleep, time in bed, number of naps, and presence of clinically-defined sleep disorders) and numerous validated questionnaires [Epworth Sleepiness Scale for excessive daytime sleepiness (EDS), Insomnia Severity Scale and Berlin Questionnaire]. Cognitive decline was defined as a difference between the MMSE and cognitive composite scores at M24 and M36 that was ranked in the lowest decile. Multivariate logistic regression models adjusted for several potential confounding factors were performed. Results: Among the 479 frail participants, 63 developed MMSE-cognitive decline and 50 cognitive composite score decrease between M24 and M36. Subjects with EDS had an increased risk of MMSE decline (OR = 2.46; 95% CI [1.28; 4.71], p = 0.007). A longer time spent in bed during night was associated with cognitive composite score decline (OR = 1.32 [1.03; 1.71], p = 0.03). These associations persisted when controlling for potential confounders. Patients with MMSE score decline and EDS had more naps, clinically-defined REM-sleep Behavior Disorder, fatigue and insomnia symptoms, while patients with cognitive composite score decline with longer time in bed had increased 24-h total sleep time duration but with higher wake time after onset. Conclusions: The risk of cognitive decline is higher in frailty subjects with EDS and longer nighttime in bed. Early detection of sleep-wake disturbances might help identifying frail subjects at risk of cognitive decline to further propose sleep health strategies to prevent cognitive impairment. http://www.clinicaltrials.gov NCT00672685; Date of registration May, 2nd 2008. [ABSTRACT FROM AUTHOR]

Poor sleep quality negatively affects memory performance, and working memory in particular. We investigated sleep habits related to sleep quality including sleep duration, daytime nap duration, nap frequency, and dream content recall frequency (DCRF). Declarative working memory can be subdivided into verbal working memory (VWM) and visuospatial working memory (VSWM). We hypothesized that sleep habits would have different effects on VWM and VSWM. To our knowledge, our study is the first to investigate differences between VWM and VSWM related to daytime nap duration, nap frequency, and DCRF. Furthermore, we tested the hypothesis that the effects of duration and frequency of daytime naps and DCRF on VWM and VSWM differed according to sex. We assessed 779 healthy right-handed individuals (434 males and 345 females; mean age: 20.7 ± 1.8 years) using a digit span forward and backward VWM task, a forward and backward VSWM task, and sleep habits scales. A correlation analysis was used to test the relationships between VWM capacity (VWMC) and VSWM capacity (VSWMC) scores and sleep duration, nap duration, nap frequency, and DCRF. Furthermore, multiple regression analyses were conducted to identify factors associated with VWMC and VSWMC scores and to identify sex-related differences. We found significant positive correlations between VSWMC and nap duration and DCRF, and between VWMC and sleep duration in all subjects. Furthermore, we found that working memory capacity (WMC) was positively correlated with nap duration in males and with sleep duration in females, and DCRF was positively correlated with VSWMC in females. Our finding of sex-related differences in the effects of sleep habits on WMC has not been reported previously. The associations between WMC and sleep habits differed according to sex because of differences in the underlying neural correlates of VWM and VSWM, and effectiveness of the sleep habits in males and females. [ABSTRACT FROM AUTHOR]

Even modest sleep restriction, especially the loss of sleep slow wave activity (SWA), is invariably associated with slower electroencephalogram (EEG) activity during wake, the occurrence of local sleep in an otherwise awake brain, and impaired performance due to cognitive and memory deficits. Recent studies not only confirm the beneficial role of sleep in memory consolidation, but also point to a specific role for sleep slow waves. Thus, the implementation of methods to enhance sleep slow waves without unwanted arousals or lightening of sleep could have significant practical implications. Here we first review the evidence that it is possible to enhance sleep slow waves in humans using transcranial direct-current stimulation (tDCS) and transcranial magnetic stimulation. Since these methods are currently impractical and their safety is questionable, especially for chronic long-term exposure, we then discuss novel data suggesting that it is possible to enhance slow waves using sensory stimuli. We consider the physiology of the K-complex (KC), a peripheral evoked slow wave, and show that, among different sensory modalities, acoustic stimulation is the most effective in increasing the magnitude of slow waves, likely through the activation of non-lemniscal ascending pathways to the thalamo-cortical system. In addition, we discuss how intensity and frequency of the acoustic stimuli, as well as exact timing and pattern of stimulation, affect sleep enhancement. Finally, we discuss automated algorithms that read the EEG and, in real-time, adjust the stimulation parameters in a closed-loop manner to obtain an increase in sleep slow waves and avoid undesirable arousals. In conclusion, while discussing the mechanisms that underlie the generation of sleep slow waves, we review the converging evidence showing that acoustic stimulation is safe and represents an ideal tool for slow wave sleep (SWS) enhancement. [ABSTRACT FROM AUTHOR]