Sleep最新文献

{"title":"Endotyping towards a better understanding of obstructive sleep apnea: heading in the right direction.","authors":"Faiza Khalid, Nicoleta Olteanu, Dennis Auckley","doi":"10.1093/sleep/zsae206","DOIUrl":"10.1093/sleep/zsae206","url":null,"abstract":"","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the bidirectional relationship between chronic kidney disease and obstructive sleep apnea.","authors":"Yu-Hsiang Lin, Kuo-Jen Lin, Jau-Yuan Chen","doi":"10.1093/sleep/zsaf002","DOIUrl":"https://doi.org/10.1093/sleep/zsaf002","url":null,"abstract":"","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress-induced increase in heart-rate during sleep as an indicator of PTSD risk among combat soldiers.","authors":"Lisa Simon, Shlomi Levi, Shachar Shapira, Roee Admon","doi":"10.1093/sleep/zsae183","DOIUrl":"10.1093/sleep/zsae183","url":null,"abstract":"<p><strong>Study objectives: </strong>Discerning the differential contribution of sleep behavior and sleep physiology to the subsequent development of posttraumatic-stress-disorder (PTSD) symptoms following military operational service among combat soldiers.</p><p><strong>Methods: </strong>Longitudinal design with three measurement time points: during basic training week (T1), during intensive stressed training week (T2), and following military operational service (T3). Participating soldiers were all from the same unit, ensuring equivalent training schedules and stress exposures. During measurement weeks soldiers completed the Depression Anxiety and Stress Scale (DASS) and the PTSD Checklist for DSM-5 (PCL-5). Sleep physiology (sleep heart-rate) and sleep behavior (duration, efficiency) were monitored continuously in natural settings during T1 and T2 weeks using wearable sensors.</p><p><strong>Results: </strong>Repeated measures ANOVA revealed a progressive increase in PCL-5 scores from T1 and T2 to T3, suggesting an escalation in PTSD symptom severity following operational service. Hierarchical linear regression analysis uncovered a significant relation between the change in DASS stress scores from T1 to T2 and subsequent PCL-5 scores at T3. Incorporating participants' sleep heart-rate markedly enhanced the predictive accuracy of the model, with increased sleep heart-rate from T1 to T2 emerging as a significant predictor of elevated PTSD symptoms at T3, above and beyond the contribution of DASS stress scores. Sleep behavior did not add to the accuracy of the model.</p><p><strong>Conclusion: </strong>Findings underscore the critical role of sleep physiology, specifically elevated sleep heart-rate following stressful military training, in indicating subsequent PTSD risk following operational service among combat soldiers. These findings may contribute to PTSD prediction and prevention efforts.</p>","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141898270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging sleep with psychiatric disorders through genetics.","authors":"Amber J Zimmerman, Struan F A Grant","doi":"10.1093/sleep/zsae235","DOIUrl":"10.1093/sleep/zsae235","url":null,"abstract":"","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal early pregnancy body mass index and risk of insomnia in the offspring.","authors":"Mia Q Zhu, Sven Cnattingius, Louise M O'Brien, Eduardo Villamor","doi":"10.1093/sleep/zsae236","DOIUrl":"10.1093/sleep/zsae236","url":null,"abstract":"<p><strong>Study objectives: </strong>To investigate the association between maternal early pregnancy body mass index (BMI) and risk of offspring insomnia.</p><p><strong>Methods: </strong>We conducted a nationwide cohort study among 3 281 803 singleton live births in Sweden born 1983-2015. Using national registries with prospectively recorded information, we followed participants for an insomnia diagnosis from 2 to up to 35 years of age. We compared insomnia risks by early pregnancy BMI categories using hazard ratios (HR) with 95% confidence intervals (CI) from adjusted Cox models. To assess unmeasured shared familial confounding, we conducted sibling-controlled analyses among 1 724 473 full siblings and studied the relation of maternal full sisters' BMI and insomnia risk in 1 185 998 offspring.</p><p><strong>Results: </strong>There were 7154 insomnia diagnoses over a median follow-up age of 17.9 years. Compared with women with normal BMI, adjusted HR (95% CI) of offspring insomnia for early pregnancy BMI categories overweight, obesity class I, and obesity classes II or III were, respectively, 1.22 (1.14, 1.30), 1.60 (1.45, 1.77), and 2.11 (1.83, 2.45). Corresponding adjusted HR (95% CI) in sibling comparisons were, respectively, 1.32 (1.05, 1.65), 1.48 (1.03, 2.14), and 1.56 (0.91, 2.65). Associations with maternal sisters' BMI were attenuated, suggesting a weak role for unmeasured shared factors. Other pregnancy, birth, and neonatal complications were associated with the risk of insomnia in offspring but did not substantially mediate the association.</p><p><strong>Conclusions: </strong>The dose-response relation between maternal overweight and obesity severity with offspring insomnia risk is not fully explained by shared familial factors.</p>","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological inhibition of histamine N-methyltransferase extends wakefulness and suppresses cataplexy in a mouse model of narcolepsy.","authors":"Fumito Naganuma, Birkan Girgin, Anne Bernadette S Agu, Kyosuke Hirano, Tadaho Nakamura, Kazuhiko Yanai, Ramalingam Vetrivelan, Takatoshi Mochizuki, Masashi Yanagisawa, Takeo Yoshikawa","doi":"10.1093/sleep/zsae244","DOIUrl":"10.1093/sleep/zsae244","url":null,"abstract":"<p><p>Histamine, a neurotransmitter, plays a predominant role in maintaining wakefulness. Furthermore, our previous studies showed that histamine N-methyltransferase (HNMT), a histamine-metabolizing enzyme, is important for regulating brain histamine concentration. However, the effects of pharmacological HNMT inhibition on mouse behavior, including the sleep-wake cycle and cataplexy, in a mouse model of narcolepsy have not yet been investigated. In the present study, we investigated the effects of metoprine, an HNMT inhibitor with high blood-brain barrier permeability, in wild-type (WT) and orexin-deficient (OxKO) narcoleptic mice. Metoprine increased brain histamine concentration in a time- and dose-dependent manner without affecting peripheral histamine concentrations. Behavioral tests showed that metoprine increased locomotor activity in both novel and familiar environments, but did not alter anxiety-like behavior. Sleep analysis showed that metoprine increased wakefulness and decreased non-rapid eye movement (NREM) sleep through the activation of the histamine H1 receptor (H1R) in WT mice. In contrast, the reduction of rapid eye movement (REM) sleep by metoprine occurred independent of H1R. In OxKO mice, metoprine was found to prolong wakefulness and robustly suppress cataplexy. In addition, metoprine has a greater therapeutic effect on cataplexy than pitolisant, which induces histamine release in the brain and has been approved for patients with narcolepsy. These data demonstrate that HNMT inhibition has a strong effect on wakefulness, demonstrating therapeutic potential against cataplexy in narcolepsy.</p>","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glymphatic system, sleep, and Parkinson's disease: interconnections, research opportunities, and potential for disease modification.","authors":"Jiri Nepozitek, Petr Dusek, Karel Sonka","doi":"10.1093/sleep/zsae251","DOIUrl":"10.1093/sleep/zsae251","url":null,"abstract":"","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Snoring and risk of dementia: a prospective cohort and Mendelian randomization study.","authors":"Yaqing Gao, Shea Andrews, Iyas Daghlas, Willa D Brenowitz, Cyrus A Raji, Kristine Yaffe, Yue Leng","doi":"10.1093/sleep/zsae149","DOIUrl":"10.1093/sleep/zsae149","url":null,"abstract":"<p><strong>Study objectives: </strong>The association between snoring, a very common condition that increases with age, and dementia risk is controversial. We aimed to investigate the observational and causal relationship between snoring and dementia, and to elucidate the role of body mass index (BMI).</p><p><strong>Methods: </strong>Using data from 451 250 participants who were dementia-free at baseline, we examined the association between self-reported snoring and incident dementia using Cox proportional-hazards models. Causal relationship between snoring and Alzheimer's disease (AD) was examined using bidirectional two-sample Mendelian randomization (MR) analysis.</p><p><strong>Results: </strong>During a median follow-up of 13.6 years, 8325 individuals developed dementia. Snoring was associated with a lower risk of all-cause dementia (hazard ratio [HR] 0.93; 95% confidence interval [CI] 0.89 to 0.98) and AD (HR 0.91; 95% CI 0.84 to 0.97). The association was slightly attenuated after adjusting for BMI, and was stronger in older individuals, APOE ε4 allele carriers, and during shorter follow-up periods. MR analyses suggested no causal effect of snoring on AD; however, genetic liability to AD was associated with a lower risk of snoring. Multivariable MR indicated that the effect of AD on snoring was primarily driven by BMI.</p><p><strong>Conclusions: </strong>The phenotypic association between snoring and lower dementia risk likely stems from reverse causation, with genetic predisposition to AD associated with reduced snoring. This may be driven by weight loss in prodromal AD. Increased attention should be paid to reduced snoring and weight loss in older adults as potential early indicators of dementia risk.</p>","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141470837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenging the paradigm of alpha-synuclein's role in disease: can low levels also be bad for you?","authors":"Stefan Clemens, Tonya N Zeczycki","doi":"10.1093/sleep/zsae229","DOIUrl":"10.1093/sleep/zsae229","url":null,"abstract":"","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accelerometer-derived sleep metrics in adolescents reveal shared genetic influences with obesity and stress in a Brazilian birth cohort study.","authors":"Marina Xavier Carpena, Karen Sanchez-Luquez, Mariana Otero Xavier, Ina S Santos, Alicia Matijasevich, Andrea Wendt, Inacio Crochemore-Silva, Luciana Tovo-Rodrigues","doi":"10.1093/sleep/zsae256","DOIUrl":"10.1093/sleep/zsae256","url":null,"abstract":"<p><p>We aimed to test the association between sleep-related polygenic scores (PGSs) and accelerometer-based sleep metrics among Brazilian adolescents and to evaluate potential mechanisms underlying the association through the enrichment of obesity, and cortisol pathway-specific polygenic scores (PRSet). Utilizing data from The 2004 Pelotas (Brazil) Birth Cohort, sleep time window and sleep efficiency were measured at the 11-year-old follow-up using ActiGraph accelerometers. Three sleep PGSs were developed based on the most recent genome-wide association study of accelerometer-based sleep measures. PRSet, calculated using variants linked to body mass index (BMI) and plasmatic cortisol concentration, aimed to assess pleiotropic effects. Linear regression models, adjusted for sex and the first 10 principal components of ancestry, were employed to explore the impact of sleep PGS and specific-PRSet on sleep phenotypes. The number of nocturnal sleep episodes-PGS was positively associated with sleep time window (β = 2.306, SE: 0.92, p = .011). Nocturnal sleep episodes were also associated with sleep time window when restricted to BMI-PRSet (β = 2.682, SE: 0.912, competitive p = .003). Both the number of sleep episodes and sleep time window cortisol-PRSets were associated (β = .002, SE: 0.001, p = .013; β = .003, SE: 0.001, p = .003, respectively) and exhibited enrichment in molecular pathways (competitive p = .011; competitive p = .003, respectively) with sleep efficiency. Sleep polygenetic components observed in European adults may partially explain the accelerometer-based sleep time window in Brazilian adolescents. Specific BMI molecular pathways strengthened the association between sleep PGS and sleep time window, while the cortisol concentration pathway had a significant impact on the genetic liability for sleep efficiency. Our results suggest genetic overlap as a potential etiological pathway for sleep-related comorbidities, emphasizing common genetic mechanisms.</p>","PeriodicalId":22018,"journal":{"name":"Sleep","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}