Sleep最新文献

Study objectives: This study examined whether sleep timing and its regularity are associated with cognitive performance in older women and whether associations vary based on cardiometabolic risk factors.

Methods: The cross-sectional analysis included 1,177 community-dwelling females (mean age 65 years) from the observational Study of Women's Health Across the Nation (SWAN) annual visit 15. Sleep timing (mean midpoint from sleep onset to wake-up) and its regularity (standard deviation of midpoint ) were assessed using actigraphy. Cognitive measures included immediate and delayed verbal memory, working memory, and processing speed. Cardiometabolic risk measures included central obesity, hypertension, diabetes, and the Atherosclerotic Cardiovascular Disease (ASCVD) risk score. Linear regression models, adjusted for covariates, tested associations between sleep and cognitive measures.

Results: After covariate adjustment, early sleep timing was associated with worse delayed verbal memory (β = -0.37; p = 0.047) and late sleep timing was associated with worse processing speed (β = -1.80; p = 0.008). Irregular sleep timing was associated with worse immediate (β = -0.29; p = 0.020) and delayed verbal memory (β = -0.36; p= 0.006), and better working memory (β = 0.50; p = 0.004). Associations between early sleep timing and delayed verbal memory strengthened as ASCVD risk increased (interaction β=-8.83, p=.026), and tsleep timing irregularity's effect on-working memory was stronger among women with hypertension (interaction β = -3.35, p = .039).

Conclusions: Sleep timing and its regularity are concurrently associated with cognitive performance in older women. Cardiovascular disease risk may modify some of these associations. Future longitudinal studies are needed to clarify these relationships.

Insomnia disorder (ID) is characterized by electroencephalographic indexes of hyperarousal, often associated with the underestimation of sleep duration (i.e., sleep state misperception). Albeit NREM sleep K-complexes (KCs) are involved in sleep protection and arousal, only a few studies investigated their alterations in ID with heterogenous findings, and results about their possible relationship with sleep state misperception are missing. The study aims to assess KCs in ID and their relationship with sleep state misperception, also considering their correlation with sleep architecture (i.e., the large-scale organization of sleep). Nineteen ID patients (12 F; age: 42.4±12.1 y) and 18 healthy controls (HC; 10 F; age: 41.6±11.9 y) underwent a night of home polysomnography and completed sleep diaries upon awakening. KC density, amplitude and area under the curve were assessed in midline frontal, central, and parietal derivations. Sleep state misperception was investigated by considering polysomnographic and subjective total sleep time (TST). We found reduced anterior KC morphology (i.e., amplitude and area under the curve) in ID patients compared to HCs, which was associated with TST underestimation. KC morphology was negatively associated with N3 latency, sleep fragmentation and arousal indexes, and positively related with N3 percentage and sleep efficiency. Our findings suggest an impaired sleep protection mechanism expressed by altered KCs morphology in ID involved in sleep state misperception. The observed correlations support the view of KC as forerunner of Slow Wave Sleep and protector of sleep continuity. A better understanding of sleep-protecting mechanisms alteration as a predisposing and/or maintaining factor of ID is needed.

Study objectives: Insufficient/irregular sleep patterns are common conditions, but their cardiovascular consequences and strategies to minimize these risks are poorly explored. We aimed to determine whether weekend sleep extension (catch-up sleep) and social jetlag may impact the incidence of subclinical atherosclerosis.

Methods: We performed a 7-day wrist actigraphy in this cohort study to monitor sleep parameters. Coronary artery calcium (CAC) was measured at two different time points. Catch-up-sleep was measured by calculating weekend minus weekday sleep duration. Social jetlag was calculated by the difference between the mean sleep midpoint on weekend days minus weekdays. The incidence of subclinical atherosclerosis was defined as baseline CAC=0, followed by CAC>0 at the follow-up. The association of incident CAC outcome was assessed using logistic regression adjusting for traditional confounders plus sleep apnea.

Results: We analyzed 1,832 participants (age: 48.8±8.0 years; 57.8% women). Incidence of CAC among subjects with catch-up sleep >90 and ≤90 minutes were 19.1% vs. 31.7%, respectively (P<0.001). In covariate-adjusted analyses (follow-up=5.4±0.90 years), we found a lower incidence of CAC in those participants with catch-up-sleep >90 minutes (OR=0.62; 95% CI 0.52-0.74). Interestingly, stratified analysis revealed that these results are modified by sleep duration (≤6.55 hours: OR=0.42; 95% CI 0.33-0.54; >6.55 hours: OR=0.96; 95% CI 0.75-1.24). In contrast, social jet lag was weakly associated with incident CAC: 0.1% increasing risk/minute.

Conclusions: Extending sleep time during the weekend is independently associated with lower 5-year CAC incidence, providing relevant insights into the cardiovascular benefits of this common sleep habit Worldwide.

Study objectives: This randomized controlled trial assessed the effects of positive airway pressure (PAP) treatment of obstructive sleep apnea (OSA) on cognition in patients with Parkinson's disease (PD).

Methods: Individuals with PD with Montreal Cognitive Assessment (MoCA) < 27 and OSA were randomized to PAP or nasal dilator strips (placebo) for 6 months. The primary outcome was the change in MoCA from baseline to 6 months compared by t-test between groups by intention to treat (ITT). Sensitivity and per protocol (PP) analyses were performed, adjusting for potential confounders. Secondary outcomes included patient-reported and motor outcomes. Exploratory outcomes comprised detailed neurocognitive tests.

Findings: We randomized 94 participants (31% female) with mean age 67.3 (SD 10.5) years, body mass index 28.1 (4·7) kg/m2 and MoCA 22.7 (3.5). The change in MoCA in the PAP group (n=48) was 0.60, 95%CI [-0.08, 1.29] and in the control group (n=46) -0.39, 95%CI [-1.21, 0.43]; between-group difference 1.00, 95%CI [-0.06, 2.05] (ITT). Adjusted ITT analyses showed improved MoCA by 1.44, 95%CI [0.09, 2.79], in treated vs. control groups. In PP analyses, the adjusted between-group difference was 1.43, 95%CI [0.054, 2.81] between PAP (n=33) vs. control (n=41) groups. Non-motor symptoms, depression and sleep quality scores, and performance on certain executive and psychomotor tasks improved with PAP. PP analyses also showed significant improvement in motor function in PAP compared to control groups.

Conclusions: Evaluation for OSA in PD patients with reduced cognition should be considered as OSA treatment may improve cognitive function, and possibly patient-reported and motor outcomes.

The National Center on Sleep Disorders Research (NCSDR) of the National Heart, Lung, and Blood Institute (NHLBI) at the National Institutes of Health (NIH) hosted a two-day virtual workshop titled Big Data Approaches for Novel Mechanistic Insights on Disorders of Sleep and Circadian Rhythms on May 2nd and 3rd, 2024. The goals of this workshop were to establish a comprehensive understanding of the current state of sleep and circadian rhythms disorders research to identify opportunities to advance the field by using approaches based on artificial intelligence (AI) and machine learning (ML). The workshop showcased rapidly developing technologies for sensitive and comprehensive remote analysis of sleep and its disorders that can account for physiological, environmental and social influences, potentially leading to novel insights on long-term health consequences of sleep disorders and disparities of these health problems in specific populations.

Study objectives: We examined associations between daily variations in objectively measured sleep and blood glucose in a sample of non-diabetic young adults to complement laboratory studies on how sleep affects blood glucose levels.

Methods: One hundred and nineteen university students underwent sleep measurement using an Oura Ring 2 and continuous glucose monitoring (CGM) for up to 14 days. In 69 individuals who consumed a standardized diet across the study, multilevel models examined associations between sleep duration, timing, efficiency, and daily CGM profiles. Separately, in 58 individuals, multilevel models were used to evaluate postprandial glycaemic responses to a test meal challenge on 7 days. Participants also underwent oral glucose tolerance testing once after a night of ad libitum sleep, and again following a night of sleep restriction by 1-2 hours relative to that individual's habitual sleep duration. Between-condition glucose and insulin excursions, HOMA-IR and Matsuda index were compared.

Results: Nocturnal sleep did not significantly influence following-day CGM profiles, postprandial glucose, or nocturnal mean glucose levels (all ps > .05). Longer sleep durations were associated with lower same-night glucose variability (all ps < .001). However, the range of variation in sugar levels was small and unlikely to be of functional significance. Considering naps in the analysis did not alter the findings. Sleep restriction by an average of 1.73 hours (SD = 0.97) did not significantly impact excursions in glucose or insulin or insulin sensitivity the following morning (all ps > .05).

Conclusions: Glucose handling in young, healthy adults may be more resilient to real-life fluctuations in sleep patterns than previously thought.

Clinical trial information: Monitoring Sleep and Glucose Among University Students https://clinicaltrials.gov/study/NCT04880629, ID: NCT04880629.

Study objectives: Disrupted nighttime sleep is common in pediatric narcolepsy type 1, yet its cognitive impact is unknown. As N2 sleep spindles are necessary for sleep-dependent memory consolidation, we hypothesized that narcolepsy type 1 impairs memory consolidation via N2 sleep fragmentation and N2 sleep spindle alterations.

Methods: We trained 28 pediatric narcolepsy type 1 participants and 27 healthy controls (HCs) on a spatial declarative memory task before a nocturnal in-lab polysomnogram and then gave them a cued recall test upon awakening in the morning. We extracted wake and sleep stage bout numbers and N2 spindle characteristics from the polysomnogram and conducted mixed model analysis of sleep-dependent memory consolidation to identify group differences.

Results: Narcolepsy type 1 participants had shorter N2 bout durations and associated shorter N2 spindles versus HC, but other N2 spindle features were similar. Narcolepsy type 1 participants had worse memory performance postsleep than HCs after adjusting for age and gender (mean memory consolidation HC: -3.1% ± 18.7, NT1: -15.6 ± 24.8, main effect group × time of testing F = 5.3, p = .03). We did not find significant relationships between sleep-dependent memory consolidation and N2 spindle characteristics. Notably, increased N1% was associated with worse sleep-dependent memory consolidation with results driven by the narcolepsy type 1 group.

Conclusions: Sleep-dependent memory consolidation is mildly impaired in youth with narcolepsy type 1 and findings may be attributed to increases in N1 sleep. Further studies are needed to determine if these findings are generalizable and reversible with sleep-based therapies.