Sleep advances : a journal of the Sleep Research Society最新文献

This study provided a preliminary examination of indices of obstructive sleep apsnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology. A total of 93 adults with DS (aged 25-61 years) from the Alzheimer Biomarker Consortium-DS completed cognitive assessments, MRI and positron emission tomography (PET) scans (assessing amyloid-beta [Aβ] and tau), and a one-night home sleep study using the WatchPAT-300 device. Study partners also reported on depressive symptoms and diagnoses. Correlational analyses examined relationships between sleep variables, PET biomarkers, and AD symptomatology (cognitive functioning and depressive mood), controlling for sociodemographics. A total of 81 participants (87 per cent) completed valid WatchPAT data. Of these, 60 (74 per cent) screened positive for OSA, and an additional 11 had a prior OSA diagnosis and used CPAP during the test night. Nearly half (45 per cent) of those screening positive for OSA had no prior diagnosis, indicating under-detection. Among the 22 participants using OSA treatment, 50 per cent continued to show sleep-disordered breathing, suggesting suboptimal treatment effectiveness. Higher wake percentage and shorter total sleep time were associated with greater Aβ and tau burden. Cognitive performance was negatively associated with wake percentage, total sleep time, and oxygenation indices (minimum oxygen, desaturation, and time ≤ 88 per cent oxygen). Depressive symptoms were negatively related to total sleep time. These findings add preliminary evidence linking sleep disruption and OSA with AD-related pathology and symptomatology. Larger, longitudinal studies are needed to confirm these associations and evaluate whether improving sleep quality and treating OSA may help delay AD onset in this high-risk population.

The mismatch between rising sleep need and the fluctuating ability to fall asleep underlies insomnia-the most common sleep disorder-yet remains poorly understood. While sleep need increases steadily with time awake, sleep propensity-the likelihood of transitioning from wake to sleep-follows a bimodal pattern, peaking in the mid-afternoon, dipping in the evening, and rising again near bedtime. Building on our previously developed wave model of sleep dynamics, we extend this homeostatic framework to the waking period and show that it predicts the observed bimodal sleep propensity curve. This pattern emerges from two interacting factors: wake-state instability, which increases exponentially across the day, and interaction strength between states, which follows a biphasic trajectory. Together, they produce a daily profile of sleep propensity that closely aligns with experimental data. Notably, the empirical curve demonstrates a deeper evening dip than the model alone predicts-reflecting the known circadian modulation of sleep propensity. The model reveals that the mid-afternoon peak reflects maximal interaction at the homeostatic equilibrium threshold, while the evening dip results from minimal coupling between sleep and wake states, counteracting high instability. A late-day rise in both factors facilitates sleep onset at bedtime and beyond. Experimental data from sleep deprivation further support these predictions. This work provides a mechanistic foundation for understanding daily sleep propensity and may inform strategies to improve sleep and performance in both health and disease.

Sleep is a vital and universal behavior distinct from mere inactivity, yet its ecological role remains poorly understood due to methodological limitations in recording sleep in the wild. Using a small, low-power biologger, collecting brain activity, body movements, and physiology, we recorded key sleep parameters in wild black rats (Rattus rattus) under semi-captive conditions. We developed a rapid (<1 h) surgical procedure using a custom subdermal flexible electrode, providing signal quality comparable to standard cortical electrodes. Our validated semi-captive setup allowed animals to remain in their natural environment with ad libitum food and social contact while minimizing interactions. This protocol enables the study of sleep's ecological role and the influence of environmental factors on sleep expression, offering insights into its evolution. Additionally, it can help clarify sleep's central role in the context of global environmental change. By monitoring general behavior and sleep patterns in four wild rats for up to 10 days post-surgery, as well as feeding behavior for over a month, we observed no signs of pain or stress, with sleep patterns stabilizing within 2 days. This approach provides a unique tool to assess sleep variability and flexibility, demonstrating its feasibility for studying sleep in small (<200 g) wild animals.

Sleep spindles are neural events unique to nonrapid eye movement sleep that play key roles in memory reactivation and consolidation. However, much of the evidence for their function remains correlational rather than causal. Closed-loop brain stimulation uses real-time monitoring of neural events (often via electroencephalography; EEG) to deliver precise auditory, magnetic, or electrical stimulation for research or therapeutic purposes. Automated online algorithms to detect and stimulate sleep spindles have recently been validated, but the time- and frequency-resolved physiological responses generated by them have not yet been documented. Building on the recent findings that sleep spindles do not block the transmission of sound to cortex, the present work investigates the neurophysiological responses to closed-loop auditory stimulation of sleep spindles. EEG data were collected from 10 healthy human adults (6 nights each), whilst sleep spindles were detected and in half the nights, targeted with auditory stimulation. Spindles were successfully stimulated before their offset in 97.6% of detections and did not disturb sleep. Comparing stimulation with sham, we observed that stimulation resulted in increased sigma activity (11-16 Hz) at about 1 second poststimulation but that stimulation occurring at the beginning of the spindle also resulted in early termination of the spindle. Finally, we observed that stimulating an evoked spindle did not elicit additional sigma activity. Our results validate the use of closed-loop auditory stimulation targeting sleep spindles, and document its neural effects, as a basis for future causal investigations concerning spindles' roles in memory consolidation.

Study objectives: Circulating non-esterified fatty acids (NEFAs) have been associated with impaired glucose metabolism but their modifiable determinants remain uncertain. We sought to determine the association between objectively-measured sleep disordered breathing (SDB), which is also associated with dysglycemia, and NEFA levels among community-dwelling older adults.

Methods: We analyzed 787 older adults who had total fasting and post-load NEFAs measured in 1996-1997 in the Cardiovascular Health Study and underwent polysomnography between 1995 and 1997 in the Sleep Heart Health Study. We used multivariable linear regression to model NEFAs as a function of four SDB parameters: apnea-hypopnea index, arousal index, hypoxemia, and slow-wave sleep, and tested formal mediating effects by insulin sensitivity estimated with the Gutt index.

Results: The mean age of study participants was 77.5 ± 4.3 years. The proportion of females and non-Hispanic whites was 58.7 per cent and 84.2 per cent, respectively. We did not find statistically significant associations between any of the SDB parameters and fasting NEFAs, but higher amounts of slow-wave sleep were significantly associated in a linear fashion with lower total post-load NEFAs in unadjusted and adjusted models [adjusted: β = -0.004, SE = 0.001, p = .02]. In mediation analyzes, 10 per cent of the slow wave sleep-NEFA association was mediated by Gutt-estimated insulin sensitivity (p = .45 for the indirect effect).

Conclusions: Among the SDB measures studied, only higher levels of objectively measured slow-wave sleep were significantly associated with lower levels of post-load NEFAs, although the underlying mechanism is uncertain. Establishing a causal link would make SDB interventions a promising target for NEFA regulation.

Study objectives: There are large individual differences in the homeostatic response to sleep deprivation, as reflected in slow wave sleep (SWS) and electroencephalogram (EEG) spectral power, which have largely been left unexplained. Recent evidence suggests the possible involvement of the activity-regulated cytoskeleton-associated protein (ARC) gene. Here we assessed the effects of the "c.*742 + 58C > T non-coding single nucleotide polymorphism" of the human ARC gene (rs35900184) on sleep-physiological and waking-neurobehavioral responses to total sleep deprivation (TSD).

Methods: N = 50 healthy, young adults participated in a 4-day/3-night in-laboratory study with a 38-h TSD period, flanked by 10-h baseline and recovery sleep opportunities. Sleep was recorded polysomnographically and the EEG of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep was subjected to spectral analysis. Waking neurobehavioral functioning was measured with the psychomotor vigilance test (PVT) and the Karolinska Sleepiness Scale (KSS).

Results: ARC C/C homozygotes, compared to T allele carriers, showed a greater SWS rebound during recovery sleep after TSD relative to baseline. ARC T/T homozygotes showed increased EEG spectral power in the NREM theta and alpha bands and in the REM delta, theta, alpha, and beta bands, but there was no significant genotype difference in the NREM delta power response to TSD. There were also no significant genotype differences in the impact of TSD on PVT performance and KSS sleepiness.

Conclusions: Individual differences in the sleep physiological rebound after TSD were influenced by ARC genotype. However, our findings were only partially consistent with ARC mediating the sleep homeostatic response to sleep deprivation. This article is part of the Genetic and Other Molecular Underpinnings of Sleep, Sleep Disorders, and Circadian Rhythms Including Translational Approaches Collection.

Study objectives: The impact of sleep loss on memory encoding is well described in adults, yet less understood in youth, despite the prevalence and educational relevance of adolescent sleep loss. Here, we implement at-home sleep restriction in youth ages 10-14 and a well-validated hippocampus-dependent learning task to elucidate how real-world levels of sleep loss affect distinct memory encoding processes at this young age.

Methods: A within-subject cross-over design involved five nights of at-home sleep restriction (7.5 h in bed) compared to sleep optimization (10 h in bed). Restriction was achieved by delaying bedtime and advancing risetime equally. All sleep was monitored with wrist actigraphy, sleep diaries, and daily calls to the laboratory. Testing involved the validated Mnemonic Similarity Task (MST), which can distinguish between two components of successful memory encoding: general memory recognition for old items and "lure discrimination," a hippocampus-dependent ability to distinguish similar yet distinct items.

Results: As estimated by actigraphy, our manipulation reduced sleep by 1.4 ± 0.48 h per night for five nights. This reduction resulted in a selective deficit in MST-indexed memory encoding; we observed a decrease in lure discrimination (i.e. the ability to distinguish highly similar items), but no impact on recognition of old items.

Conclusions: We present evidence that low levels of sleep loss for five nights (typical of a school week) are sufficient to alter memory encoding in youth. We interpret these data in the context of classroom-based learning and speculate that reduced lure discrimination may yield memory that is less capable of distinguishing closely related facts and concepts.

Study objectives: To examine whether there is a temporal association between sleep disturbance and multimorbidity.

Methods: We performed a cross-sectional and longitudinal observational analysis in people aged 40 years or more, recruited from the knee pain and related health in the community cohort study. The primary exposure was the Sleep Problems Index II score in tertiles measured at baseline. The primary outcome was count of chronic conditions developed in 5 years. Pain, low mood, and anxiety were measured at 2 years as mediators. Poisson regression was used to calculate adjusted relative risk and 95% confidence intervals.

Results: We included 4488 participants in the cross-sectional analysis at baseline and 1941 in the 5-year longitudinal analysis. At baseline, the adjusted relative risks for prevalent multimorbidity were 1 (reference) for tertile 1, 1.09 (95% confidence interval; 1.01-1.18) for tertile 2, and 1.21 (95% confidence interval; 1.11-1.32) for tertile 3 of the sleep disturbance score (p for trend <.001). Of the total association between sleep disturbance and multimorbidity, 14 per cent (95% confidence interval; 9% to 19%) were mediated by pain and 7 per cent (95% confidence interval; 2% to 13%) by low mood. In the 5 year follow-up, the adjusted relative risk for incident multimorbidity were 1 (reference) for tertile 1, 1.12 (95% confidence interval; 0.98-1.28) for tertile 2, and 1.25 (95% confidence interval; 1.06-1.47) for tertile 3 (p for trend .007). Of the total association between sleep disturbance and multimorbidity, 10 per cent (95% confidence interval; 2% to 18%) was mediated by pain.

Conclusions: Sleep disturbance is associated with multimorbidity. The association is dose-dependent, temporal, and partially mediated by pain.

Study objectives: Diverse studies have reported longer sleep durations and later circadian timing during the initial COVID-19 lockdown period. Little is known about whether effects persisted after 2020. This analysis addresses three questions: (1) How did sleep timing and duration change from 2017 to 2023? (2) Did working from home explain trends? (3) Did effects differ by education, income, or race/ethnicity groups?

Methods: The American Time Use Survey is a nationally representative survey conducted by the US Bureau of Labor Statistics that collects 24-hour time diaries. These data are used to identify respondents who worked on the sampled day, their work location (home or not), and three sleep variables: wake-up time, bedtime, and 24-hour sleep total. Ordinary least squares regression is used to answer the study questions, comparing the COVID time period (May 2020 to December 2023) to PRECOVID (January 2017 to March 2020).

Results: Sleep duration was longer in the COVID time period compared to PRECOVID, by 0.23 hours (95% confidence interval = 0.17, 0.29), with earlier average bedtimes and later average waking times. There were no significant secular trends in sleep outcomes within the COVID time period, suggesting that these changes have continued through 2023. Controlling for working from home modestly attenuated, but did not eliminate, the COVID effects. Effects were generally similar across sociodemographic groups.

Conclusions: COVID-related changes in sleep for working adults in the United States, specifically later circadian timing and increased duration, seem to be sustained through 2023.