Neurobiology of Sleep and Circadian Rhythms最新文献

{"title":"Sleep and immune health: How dogs, goats and ‘factor S’ shaped a field","authors":"Mark R. Opp ,&nbsp;Luca Imeri","doi":"10.1016/j.nbscr.2025.100118","DOIUrl":"10.1016/j.nbscr.2025.100118","url":null,"abstract":"<div><div>Chronic insufficient sleep kills! Although this statement has high ‘face validity’, it is only recently that empirical evidence existed to support it. There are now sufficient data for numerous meta-analyses and systematic reviews to demonstrate that chronic insufficient sleep is associated with many inflammatory pathologies that are a public health burden. As a result, it is now well accepted that sleep is important for physical and mental health. This awareness derives from research that began in the late 19th and early 20th centuries and continues to the present day. In this narrative review we trace this rich history within the context of the research contributions of Professor James Krueger and his colleagues. The historic and current research by Professor Krueger and colleagues is fundamental to the many ongoing pre-clinical and clinical research programs focused on all aspects of sleep and immune health.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100118"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep and circadian disorders as risk factors for autoimmune disease: A population-based study","authors":"Amber R. Li ,&nbsp;Bhaavyaa Shah ,&nbsp;Michael L. Thomas ,&nbsp;Michael J. McCarthy ,&nbsp;Alejandro D. Meruelo","doi":"10.1016/j.nbscr.2025.100129","DOIUrl":"10.1016/j.nbscr.2025.100129","url":null,"abstract":"<div><h3>Background</h3><div>Sleep and circadian disruption have been increasingly linked to immune dysregulation, yet population-level associations with autoimmune disease remain underexplored. We examined whether delayed sleep phase disorder (DSPD), obstructive sleep apnea (OSA), primary insomnia, and hypersomnia were associated with autoimmune conditions in a large, diverse U.S. cohort.</div></div><div><h3>Methods</h3><div>Data were drawn from the All of Us Research Program Registered Tier Dataset v8. Participants were categorized into sleep disorder groups based on clinical diagnoses, with regular sleepers serving as controls. Autoimmune disease was defined using SNOMED-coded records. DSPD and primary insomnia were analyzed using rare disease logistic regression; OSA and hypersomnia were analyzed using 1:5 propensity score matching. Adjusted logistic regression models included age, sex at birth, race, ethnicity, income, BMI, and chronic inflammatory diagnosis. E-values assessed robustness to unmeasured confounding.</div></div><div><h3>Results</h3><div>All four sleep disorder groups showed significantly higher odds of autoimmune diagnosis relative to regular sleepers (p &lt; 2.2 × 10⁻¹⁶). Adjusted odds ratios were: DSPD (OR = 0.26; 95 % CI: 0.15–0.45), OSA (OR = 0.46; 95 % CI: 0.41–0.52), primary insomnia (OR = 0.46; 95 % CI: 0.41–0.52), and hypersomnia (OR = 0.48; 95 % CI: 0.46–0.50). Older age, female sex, and chronic inflammation were associated with higher autoimmune prevalence. Asian race and BMI were inversely associated with autoimmune risk; higher income was unexpectedly associated with greater autoimmune diagnosis.</div></div><div><h3>Conclusions</h3><div>Distinct sleep phenotypes were associated with autoimmune conditions. These associations may reflect shared or bidirectional links between sleep disruption and immune dysregulation.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100129"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The cell-intrinsic circadian clock is dispensable for lateral posterior clock neuron regulation of Drosophila rest-activity rhythms","authors":"Charlene Y.P. Guerrero,&nbsp;Madelyn R. Cusick,&nbsp;Amanda J. Samaras,&nbsp;Natalie S. Shamon,&nbsp;Daniel J. Cavanaugh","doi":"10.1016/j.nbscr.2025.100124","DOIUrl":"10.1016/j.nbscr.2025.100124","url":null,"abstract":"<div><div>Circadian control of behavior arises from intercommunication among a distributed network of circadian clock neurons in the brain. Single-cell sequencing and brain connectome data support the division of the ∼240 brain clock neurons in <em>Drosophila</em> into ∼20 subclusters, and functional studies demonstrate that these populations differentially contribute to behavioral outputs. Here, we have used genetic tools that enable highly selective, cell-specific manipulations to investigate the role of molecular clock function and neuronal activity within the lateral posterior clock neurons (LPNs) in the regulation of rest-activity rhythms. We find that genetic silencing of these neurons, which compromises signaling with downstream neuronal targets, substantially reduces the strength of free-running rest-activity rhythms. In contrast, locomotor activity patterns are robust to CRISPR-mediated disruption of molecular clock cycling within the LPNs. We conclude that the LPNs act as driven oscillators that retain the capacity to transmit circadian information in the absence of cell-intrinsic molecular clocks.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100124"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143892214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergies from a distance: Inspirations from the struggles of Dr James M Krueger","authors":"William A. Banks","doi":"10.1016/j.nbscr.2025.100114","DOIUrl":"10.1016/j.nbscr.2025.100114","url":null,"abstract":"<div><div>In this article for Dr Krueger's Festschrift, I trace how his early career influenced many aspects in the fields of sleep, neuroimmunology, and the microbiome. Mostly, however, I trace how his career and interests intertwined with those of Abba J. Kastin and mine and how he exerted a profound influence on the direction of our studies. Dr. Krueger, while developing his career as a sleep researcher, encountered resistance to his work that required two major paradigm shifts: 1) that bacterial products could affect sleep and 2) that small peptides can cross the blood-brain barrier (BBB) in sufficient amounts to affect brain functioning. Dr Kastin had also shown that small peptides administered peripherally could affect brain function and postulated that this was because they could cross the BBB. Our efforts to determine whether peptides could or could not cross the BBB were bolstered by Dr Krueger's exemplary struggles.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection","authors":"Mark R. Zielinski ,&nbsp;Sean D. Carey ,&nbsp;John A. Craig","doi":"10.1016/j.nbscr.2025.100121","DOIUrl":"10.1016/j.nbscr.2025.100121","url":null,"abstract":"<div><div>Evidence indicates relationships between sleep and the innate immune system during homeostatic sleep and sleep responses after infection. The innate immune system and sleep-like states are highly conserved between simple species and more complex species such as humans. A wide variety of bacteria, viruses, and parasites change sleep patterns in the host during infection. The effects of infection on sleep can occur, in part, due to the bolus and route of infection, prior exposure, immune status of the individual/organism, and the type of pathogen. In addition, elements of circadian patterns and sleep prior to and after infection can modulate the infection pathology and resolution. Innate immune molecules, such as the cytokines interleukin-1 beta and tumor necrosis factor-alpha, fluctuate with the time of day of increased activity and sleep propensity, increase in response to increased waking activity from sleep loss, and are altered from infection by bacteria and viruses to alter sleep and the electroencephalogram. This review focuses innate immune mechanisms of how pathogen recognition receptors, pathogen-associated molecular patterns and danger-associated molecular patterns, energy-related molecules, oxidative stress, and inflammasomes are activated with infection to potentially affect sleep.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100121"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"No association between chronotype and cardiovascular response to a cognitive challenge in the morning using a Bayesian approach","authors":"Larissa N. Wüst ,&nbsp;Christian Cajochen ,&nbsp;Ruta Lasauskaite","doi":"10.1016/j.nbscr.2025.100125","DOIUrl":"10.1016/j.nbscr.2025.100125","url":null,"abstract":"<div><div>A chronotype is defined as a preference for certain behaviours (e.g., sleep and wake) to occur at specific times of day. It is therefore also temporally linked with cognitive performance across the day. In an exploratory analysis, we sought to find associations between chronotypes determined from self-reported habitual sleep timing and from salivary melatonin onset with mental effort during a 2-back working memory task. Mental effort was operationalized as sympathetic beta-adrenergic impact on the heart, which is best reflected by the cardiac pre-ejection period (PEP) and also influences systolic blood pressure (SBP). Each participant underwent two experimental sessions in the morning: once after sleeping for 8 h and once after sleeping for 5 h the night before. To determine the timing of evening melatonin onset, participants took saliva samples at hourly intervals at home in the evening, prior to their experimental sessions. Chronotypes were determined using reported sleep times from the Munich Chronotype Questionnaire and average melatonin onset during both sleep conditions. Based on this, participants were grouped into early, intermediate, or late types. Neither alertness (<em>BF</em>_<em>10</em> = 0.019), perceived task demand (<em>BF</em>_<em>10</em> = 0.008), nor SBP response (<em>BF</em>_<em>10</em> = 0.268) were credibly impacted by sleep-time derived chronotype, while the association with PEP response (<em>BF</em>_<em>10</em> = 0.631) during a cognitive challenge in the morning was inconclusive. Similarly, the timing of evening melatonin onset did not affect alertness (<em>BF</em>_<em>10</em> = 0.003), perceived task demand (<em>BF</em>_<em>10</em> = 0.006), or PEP or SBP response (PEP: <em>BF</em>_<em>10</em> = 0.232, SBP: <em>BF</em>_<em>10</em> = 0.263) during the cognitive challenge. Our data shows no impact of chronotypes on effort-related cardiovascular response during a cognitive challenge in the morning, which was scheduled according to habitual sleep times.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100125"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep in disease: inflammation and chronic rhinosinusitis","authors":"Vivek C. Pandrangi ,&nbsp;Jeremiah A. Alt","doi":"10.1016/j.nbscr.2025.100120","DOIUrl":"10.1016/j.nbscr.2025.100120","url":null,"abstract":"<div><div>Chronic rhinosinusitis (CRS) is a common inflammatory disorder that is associated with significant quality of life (QOL) impairment, including sleep dysfunction. There are multiple factors that have been independently associated with poor sleep among this population including alterations in inflammatory mediators, rhinologic symptom interference such as nasal discharge, obstruction, and facial pain, and co-morbid conditions including asthma. While there is a high prevalence of sleep dysfunction among this population, treatment with both medical and surgical options may lead to sustained improvements in sleep. This review aims to highlight the burden of sleep dysfunction, discuss common theories regarding the etiology, and evaluate strategies that may facilitate improvement in sleep dysfunction among patients with CRS.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100120"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic signals in sleep regulation: the role of brown adipose tissue","authors":"Éva Szentirmai ,&nbsp;Levente Kapás","doi":"10.1016/j.nbscr.2025.100122","DOIUrl":"10.1016/j.nbscr.2025.100122","url":null,"abstract":"<div><div>The regulation of sleep, while primarily attributed to the interplay between circadian and homeostatic processes, is significantly influenced by a multitude of additional factors that profoundly impact sleep quantity and quality. These factors encompass both external environmental stimuli, such as ambient temperature and somatosensory inputs, and internal physiological changes. The intricate relationship between metabolism and sleep has been a subject of extensive research, with particular attention given to the role of metabolic signals in sleep regulation. Among these, the brown adipose tissue (BAT) has emerged as a key player, studied from various perspectives including its physiological responses to sleep deprivation, its effects on sleep when activated, the consequences of impaired BAT thermogenesis on sleep patterns, and its metabolic activity across different sleep states. The cumulative evidence from these investigations suggests that BAT plays a crucial role in maintaining an optimal metabolic environment conducive to sleep, a function that becomes particularly significant in contexts of prior sleep loss, inflammatory conditions, and fluctuations in ambient temperature.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100122"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of traumatic brain injury severity and sex on sleep architecture, duration, and fragmentation","authors":"Grant S. Mannino ,&nbsp;Tabitha R.F. Green ,&nbsp;Sean M. Murphy ,&nbsp;Michael R. Sierks ,&nbsp;Mark R. Opp ,&nbsp;Rachel K. Rowe","doi":"10.1016/j.nbscr.2025.100127","DOIUrl":"10.1016/j.nbscr.2025.100127","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is frequently associated with acute and chronic disturbances in sleep architecture. However, the extent to which injury severity and biological sex influence post-traumatic sleep patterns remains underexplored in preclinical models. Here, we used a validated, noninvasive piezoelectric monitoring system to assess sleep in male and female mice following sham (n = 30), mild (n = 32), or moderate (n = 32) midline fluid percussion injury (mFPI). Physiological parameters were recorded non-invasively to determine sleep for 48 h post-injury. Hierarchical mixed-effects models were used to evaluate effects of injury severity and sex on sleep duration, architecture, and fragmentation. We found that sleep increased during the acute post-injury period regardless of TBI severity, but that sleep fragmentation was selectively elevated after moderate injury. Notably, female mice exhibited greater overall sleep disturbances compared to males, highlighting a sex-dependent vulnerability. These effects varied across the light-dark cycle. This study provides the first detailed characterization of sex- and severity-specific changes in sleep architecture and fragmentation following diffuse TBI using a high-throughput, noninvasive method. Importantly, it reveals that injury severity predicts the extent of sleep fragmentation highlighting a direct link between injury severity and disrupted sleep architecture. These findings contribute to the growing recognition of sleep fragmentation as a relevant biomarker in TBI and establish a framework for future mechanistic and interventional studies.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100127"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial depletion and repopulation differentially modulate sleep and inflammation in a mouse model of traumatic brain injury","authors":"Katherine R. Giordano ,&nbsp;Tabitha R.F. Green ,&nbsp;Mark R. Opp ,&nbsp;Rachel K. Rowe","doi":"10.1016/j.nbscr.2025.100115","DOIUrl":"10.1016/j.nbscr.2025.100115","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) causes persistent sleep disturbances, leading to long-term neurological consequences and reduced quality of life. We hypothesized that microglial depletion via PLX5622 (PLX), a colony-stimulating factor 1 receptor (CSFR1R) inhibitor, would exacerbate sleep disturbances and alter inflammatory profiles after TBI, and that microglial repopulation would ameliorate these effects. Male mice received PLX or control diets (21 days) followed by a midline fluid percussion injury (mFPI) or sham surgery. Physiological parameters were recorded non-invasively to determine sleep for 7 days post-injury. Subsequently, PLX was withdrawn to allow microglial repopulation, and sleep was assessed during the 7-day repopulation period. In a subset of mice, repeated blood draws were taken to quantify sleep regulatory cytokine concentrations (interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α). TBI significantly reduced sleep in mice on a control diet during the light period (3, 5, and 7 days post-injury), but not the dark period. In PLX-treated mice, TBI did not alter sleep in the light period, however, sleep in the dark period was increased at 3 days post-injury. During the microglial repopulation period, PLX-treated TBI mice slept significantly more in the dark period compared to PLX sham mice and sleep was similar in control TBI vs PLX TBI mice. Analyses revealed that elimination of microglia did not alter baseline cytokine levels. IL-6 was elevated in PLX TBI mice at 1 and 7 days post-injury compared to TBI mice on control diet, while IL-1β and TNF-α remained unchanged. This study highlights the critical role of microglia in modulating post-TBI sleep and inflammation. Findings suggest differential effects of TBI on sleep depending on microglial depletion or repopulation status, with IL-6 serving as a marker of the inflammatory response in microglia-depleted conditions.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100115"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}