Nature and Science of Sleep最新文献

Objective: Sleep disorders are common in Alzheimer's disease (AD) patients and can impair the glymphatic system, leading to cognitive decline. This study aimed to investigate whether AD patients with sleep disorders exhibit worse glymphatic function and more severe cognitive impairment compared to those without sleep disorders and to explore the underlying molecular imaging mechanisms.

Methods: This study included 40 AD patients with sleep disorders (ADSD), 39 cognitively matched AD patients without sleep disorders (ADNSD), and 25 healthy middle-aged and elderly controls (NC). Participants underwent functional magnetic resonance imaging (fMRI), and cognitive and sleep assessments. The ALPS (Along the Perivascular Space) index was calculated, followed by intergroup comparisons, correlation analyses, and mediation analyses. The diagnostic utility of the ALPS index was assessed using a receiver operating characteristic (ROC) curve.

Results: The ALPS index was lower in the ADNSD and ADSD groups compared to the NC group. In the ADSD group, PSQI scores were negatively correlated with MMSE scores. The ALPS index was positively correlated with MMSE scores and negatively with PSQI scores. Mediation analyses indicated that the ALPS index partially mediated the effect of sleep disturbances on cognitive impairment (indirect effect = -0.134; mediation effect = 30.505%). The area under the ROC curve (AUROC) for distinguishing ADSD from ADNSD was 0.86, with a cutoff ALPS index value 1.309.

Conclusion: Sleep disorders worsen glymphatic function and cognitive impairment in AD patients. The ALPS index partially mediates the impact of sleep disorders on cognitive function and shows moderate accuracy in distinguishing between patients with ADSD and ADNSD.

Purpose: It is presumed by many that acute sleep loss results in degraded in-game esports (competitive, organized video game play) performance. However, this has not been experimentally investigated to date. The objective of the current experiment was to elucidate whether ~29hrs of total sleep deprivation impacts in-game performance for the popular esport Rocket League.

Patients and methods: Twenty skill-matched pairs (N = 40 total) were recruited. Within each pair, one participant was assigned to an intervention group (TSD), while the other was assigned to a control group (CON). Two test sessions occurred; one while both participants were rested (baseline), and the other while the CON participant was rested but the TSD participant was sleep deprived (experimental).

Results: Following total sleep deprivation, TSD participants reported higher Karolinska Sleepiness Scale-measured subjective sleepiness and lower subjective alertness and motivation, as well as worsened PVT response speed and ~5 times greater PVT lapse incidence, and worsened response speed on a two-choice categorization task. However, overall in-game Rocket League performance did not worsen due to total sleep deprivation. Exploratory analyses of performance indicators suggest a potential shift toward a simpler and safer strategy following sleep deprivation.

Conclusion: Following a bout of ~29hrs total sleep deprivation, overall in-game Rocket League performance remained unaffected. This presents as a promising finding given the high potential for acute pre-competition sleep disturbance in esports, though habitual sleep remains a concern for esport athletes.

Purpose: Numerous studies have identified a correlation between sleep and delirium; however, the causal relationship remains ambiguous. This bidirectional two-sample Mendelian randomization (MR) study was conducted to examine the possible causal relationships between sleep traits and delirium.

Patients and methods: Utilizing genome-wide association studies (GWAS), we identified ten sleep traits: chronotype, sleep duration, short sleep duration, long sleep duration, daytime napping, daytime sleepiness, insomnia, number of sleep episodes (NSE), sleep efficiency, and rapid eye movement sleep behavior disorder (RBD). In this MR study, genetic variants independently associated with exposures were selected as instrumental variables (IVs). To establish causal inferences, three regression models were employed-inverse variance weighted (IVW), MR Egger, and weighted median (WM) -and conducted sensitivity analyses to assess the robustness of our findings.

Results: Our results suggest no significant causal association between the ten sleep traits and the risk of delirium. The reverse MR analysis revealed that delirium is associated with an increased propensity for morning chronotype [OR_IVW, 1.025; 95% CI, 1.012-1.036; p = 1.50E-05; adjusted p values (p_adjusted)= 1.35E-04] and a decreased risk of long sleep duration [OR_IVW, 0.996; 95% CI, 0.993-0.999; p = 0.013; p_adjusted= 0.059]. However, no robust evidence currently exists to substantiate a causal relationship between delirium and other sleep traits.

Conclusion: Our bidirectional, two-sample MR analysis study did not provide definitive evidence that sleep traits may augment the susceptibility to delirium. However, the reverse MR results indicate that delirium may predispose patients to an earlier sleep-wake cycle. Additional large-scale investigations are necessary to examine the bidirectional causality between delirium and sleep traits.

Purpose: Aimed to analyze the developmental characteristics of craniofacial structures and soft tissues in children with obstructive sleep apnea (OSA) and to establish and evaluate prediction model.

Methods: It's a retrospective study comprising 747 children aged 2-12 years (337 patients and 410 controls) visited the Department of Otolaryngology-Head and Neck Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University (July 2017 to March 2024). Lateral head radiographs were obtained to compare the cephalometric measurements. The clinical prediction model was constructed using LASSO regression analysis. We analyzed 300 children from the Xi'an Children's Hospital for external validation.

Results: Children with OSA had a higher body mass, a higher tonsil grade, larger AN ratio (ratio of the adenoids to the skeletal upper airway width), larger radius of the tonsils, a smaller angle between the skull base and maxilla (SNA) and smaller angle between the skull base and mandible (SNB), a larger distance from the hyoid to the mandibular plane (H-MP) and smaller distance between the third cervical vertebra and hyoid (H-C), a larger thickness of the soft palate (SPT) and smaller inclination angle of the soft palate than those of the controls (all p < 0.05). A prediction model was constructed for 2-12 years group (AUC of 0.812 [95% CI: 0.781-0.842]). Age-specific prediction models were developed for preschool children (AUC of 0.769 [95% CI: 0.725-0.814]), for school-aged children (AUC of 0.854 [95% CI: 0.812-0.895]).

Conclusion: Our study findings support the important role of craniofacial structures such as the hyoid, maxilla, mandible, and soft palate in pediatric OSA. Age-stratified predictive models for pediatric OSA indicated varying parameters across different age groups which underscore the necessity for stratifying by age in future research. The prediction model designed will greatly assist health care practitioners with rapidly identifying.

Purpose: Obstructive sleep apnea (OSA) is a contributing factor to nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the clinical and polysomnographic characteristics of OSA patients with and without NAFLD, focusing on the relationships between sleep fragmentation, arousal and NAFLD.

Materials and methods: We consecutively enrolled patients who underwent polysomnography, anthropometry, blood sampling, and abdominal ultrasonography. Patients were categorized into NAFLD and non-NAFLD groups. A comparative analysis of clinical and polysomnographic profiles was conducted, followed by multivariate binary logistic regression to explore the relationship between sleep disturbance indices and NAFLD.

Results: A total of 403 subjects were included, including 92 patients with NAFLD and 311 with non-NAFLD. NAFLD patients exhibited a greater apnea-hypopnea index (AHI) (51.19/h vs 33.60/h, p = 0.002) and oxygen desaturation index (ODI) (37.90/h vs 21.40/h, p=0.034) compared to non-NAFLD patients. Specifically, NAFLD patients had a higher rapid eye movement (REM)-AHI (53.70/h vs 43.60/h, p=0.001) and greater arousal index (AI) (32 vs 25, p = 0.009). Additionally, sleep latency (SL) was significantly lower in the NAFLD group (p < 0.05). Multivariate logistic regression analysis confirmed that REM-AHI (OR=1.023, p = 0.024), AI (OR=1.140, p = 0.01), and SL (OR=0.956, p = 0.035) were significantly associated with NAFLD in OSA patients.

Conclusion: This study revealed that sleep disturbance indices, especially AI, REM-AHI and SL, were closely related to NAFLD. When evaluating whether OSA patients are complicated with NAFLD, more attention should be given to sleep fragmentation and arousal.

Purpose: Intermittent hypoxia (IH), a defining feature of obstructive sleep apnea (OSA), is associated with heart damage and linked to transient receptor potential canonical channel 5 (TRPC5). Nonetheless, the function of TRPC5 in OSA-induced cardiac injury remains uncertain. For this research, we aimed to explore the role and potential mechanism of TRPC5 in cardiomyocyte injury induced by intermittent hypoxia.

Methods: 30 patients with newly diagnosed OSA and 30 patients with primary snoring(PS) were included in this study. Participants were subjected to polysomnography (PSG) for OSA diagnosis. Echocardiography was used to evaluate the structure and function of the heart, while peripheral blood samples were obtained. Additionally, RT-qPCR was utilized to quantify the relative expression level of TRPC5 mRNA in peripheral blood. H9c2 cells experienced IH or normoxia. TRPC5 levels in H9c2 cells were determined via RT-qPCR and Western blotting (WB) methods. H9c2 cells overexpressing TRPC5 were subjected to either normoxic or intermittent hypoxia conditions. Cell viability was determined by CCK8, the apoptosis rate, reactive oxygen species(ROS) levels, and Ca²⁺ concentration were assessed by flow cytometry, and the protein levels of TRPC5, Bcl-2, Bax, and Caspase-3 were analyzed by WB. Mitochondrial membrane potential(MMP), mitochondrial membrane permeability transition pore(mPTP), and transmission electron microscopy(TEM) were employed to observe mitochondrial function and structure. After inhibiting ROS with N-acetylcysteine (NAC), apoptosis, mitochondrial function and structure, and the concentration of Ca²⁺ were further detected.

Results: TRPC5 and left atrial diameter (LAD) were higher in OSA individuals, while the E/A ratio was lower(all P<0.05). IH impaired cell viability, triggered cell apoptosis, and enhanced TRPC5 expression in H9c2 cells(all P<0.05). The effects of IH on apoptosis, cell viability, mitochondrial function and structure damage, and oxidative stress (OxS) in H9c2 cells were accelerated by the overexpression of TRPC5(all P<0.05). Furthermore, cell apoptosis and mitochondrial structural and functional damage caused by overexpression of TRPC5 were attenuated by ROS inhibition.

Conclusion: TRPC5 is associated with structural and functional cardiac damage in patients with OSA, and TRPC5 promotes IH-induced apoptosis and mitochondrial damage in cardiomyocytes through OxS. TRPC5 may be a novel target for the diagnosis and treatment of OSA-induced myocardial injury.

Objective: To investigate whether self-reported symptoms of obstructive sleep apnea (OSA), including snoring, snorting/stopping breathing, and sleepiness, are associated with increased risk of kidney stones.

Methods: This cross-sectional study was conducted based on the 2015-2020 National Health and Nutrition Examination Survey (NHANES). Self-reported symptoms of OSA and history of kidney stones were diagnosed via questionnaires. Multivariable logistic regression was used to determine the associations between self-reported symptoms of OSA and kidney stones. Subgroup analyses and interaction tests were performed to address this issue further.

Results: A total of 9,973 participants were enrolled, and the prevalence of kidney stones was 10.76%. Although no significant association was observed between frequent snoring and kidney stones after covariate adjustments (OR 1.033, 95% CI 0.726, 1.469 p = 0.850), frequent snorting/stopping breathing was associated with a greater risk of kidney stones after covariate adjustments (OR 1.655, 95% CI 1.262, 2.172, p = 0.002). Participants who often or almost always felt sleepy also had a greater risk of kidney stones after covariate adjustment (OR 1.651, 95% CI 1.222, 2.229; p = 0.004). The interaction tests suggested that marital status (p = 0.015) and smoking status (p < 0.001) significantly interacted with the association between snorting/stopping breathing and kidney stones.

Conclusion: Self-reported frequent snorting/stopping breathing and sleepiness may be associated with increased risk of kidney stones. Although these findings may emphasize prevention of kidney stones in these people, further research was still needed to verify our results.

Background: Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder characterized by recurrent upper airway collapse and obstruction, leading to reduced or absent breathing during sleep, especially rapid eye movement (REM) sleep, and continuous positive airway pressure treatment (CPAP) is often used for treatment of OSA. Sawtooth waves (STWs) are a characteristic of REM sleep.

Objective: To examine effects of CPAP treatment on STWs during REM sleep in the OSA patients.

Methods: Polysomnographic recordings were performed on 20 moderate-to-severe OSA patients and 16 normal controls, and comparisons of STWs during REM sleep in the OSA patients with and without CPAP treatment (paired t-test or Wilcoxon signed-rank test wherever appropriate), and between OSA patients and normal controls (Student's t-test or Wilcoxon rank-sum test) were carried out. In addition, linear correlation analyses were used to estimate the relationship of STWs and REM sleep with duration of non-REM (NREM) sleep stage 3 (N3).

Results: The STWs were classified to be apnea/hypopnea associated and not associated (isolated), and the amplitude of the isolated STWs was significantly higher than that of the apnea/hypopnea associated. With CPAP treatment, the percentage of REM sleep with STWs and the amplitude of STWs were significantly increased to the levels, which were not significantly different from those in the normal controls, while the frequency of STWs was not significantly changed. In addition, the total duration of REM sleep and the duration of REM sleep with STWs were both positively correlated with the duration of N3 sleep in the normal controls and the OSA patients with CPAP treatment. Furthermore, CPAP treatment also caused a significant increase in the duration of rapid eye movements in REM sleep.

Conclusion: These findings suggest that there are some interconnections between NREM and REM sleep, and STWs not only represent the quality of REM sleep but also are correlated with N3 sleep.

Purpose: Sleep apnea (SA), associated with absent neural output, is characterised by recurrent episodes of hypoxemia and repeated arousals during sleep, resulting in decreased sleep quality and various health complications. Mitochondrial DNA copy number (mtDNA-CN), an easily accessible biomarker in blood, reflects mitochondrial function. However, the causal relationship between mtDNA-CN and SA remains unclear. This study aimed to investigate the causality between mtDNA-CN and SA while identifying potential mediating brain imaging phenotypes (BIPs).

Methods: Two-sample bidirectional Mendelian randomisation (MR) analysis was performed to estimate the causal relationship between mtDNA-CN and SA, with further validation using Bayesian framework-based MR analysis. A two-step approach was employed to evaluate causal relationships between BIPs, mtDNA-CN and SA, utilising the "product of coefficients" method to assess the mediating effects of BIPs. Multiple testing errors were corrected using the Benjamini-Hochberg method.

Results: Genetically predicted mtDNA-CN had a negative causal effect on SA (OR = 0.859, 95% CI = 0.785-0.939, P = 3.20×10^-4), whereas SA did not have a causal effect on mtDNA-CN (OR = 1.0056, 95% CI = 0.9954-1.0159, P = 0.2825). Among 3935 BIPs, two features related to white matter microstructure served as partial mediators: the second eigenvalue from diffusion MRI data analysed by tract-based spatial statistics in the right posterior thalamic radiation, with a mediation proportion of 11.37% (P = 0.0450), and fractional anisotropy in the right sagittal stratum, with a mediation proportion of 12.79% (P = 0.0323).

Conclusion: This study demonstrated a causal relationship between mtDNA-CN and SA, with specific brain white matter microstructure phenotypes potentially acting as mediators. These findings highlight the potential of mtDNA-CN as a biomarker for SA and underscore its relevance in guiding future therapeutic strategies targeting mitochondrial health and brain white matter microstructure.

Background: OSA can cause cognitive impairment (CI). The aim of this study was to investigate whether miR-20a-5p in exosomes derived from bEnd3 cells with IH mediates intercellular crosstalk and induces CI through hippocampal neuronal cell pyroptosis.

Materials and methods: BEnd3-derived exosomes were isolated from the normal oxygen control group (NC-EXOS) and IH group (IH-EXOS). In vitro, exosomes were cocultured with HT22 cells. Meanwhile, in vivo, exosomes were injected into mice via the caudal vein. The spatial memory ability of mice was tested by MWM method to evaluate the effect of exosomes on the cognitive function of mice. Adults diagnosed with OSA underwent the MoCA and ESS tests to assess cognitive function and daytime sleepiness. Spearman's rank correlation analysis was used to evaluate the correlation between miR-20a-5p and candidate proteins and clinical parameters. Transfection using small interfering RNAs, miRNA mimics, and plasmids to evaluate the role of miR-20a-5p and its target genes. Dual luciferase reporter gene assay was used to confirm the binding of miR-20a-5p to its target gene.

Results: IH could cause pyroptosis and inflammation in bEnd3 cells, and promote the expression of miR-20a-5p. Isolated IH-EXOS induced increased pyroptosis and activation of inflammatory response in vitro and in vivo, accompanied by increased expression of miR-20a-5p. In addition, IH-EXOS led to decreased learning and memory ability in mice. Interestingly, AHI was higher and MoCA scores were lower in severe OSA compared to healthy comparisons. In addition, miR-20a-5p and GSDMD were positively correlated with AHI but negatively correlated with MoCA in severe OSA. IH-induced exosomes were rich in miR-20a-5p, and these exosomes were found to deliver miR-20a-5p to HT22 cells, playing a key role in the induction of OSA-CI by directly targeting MFN2.

Conclusion: Exosome miR-20a-5p from IH-stimulated bEnd3 cells can promote OSA-CI by increasing HT22 cells pyroptosis through its target MFN2.