Neurobiology of Sleep and Circadian Rhythms最新文献

{"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}

{"title":"Foreword: Festschrift in honor of JM Krueger's research","authors":"Mark R. Opp ,&nbsp;Rachel K. Rowe ,&nbsp;Hans P.A. Van Dongen","doi":"10.1016/j.nbscr.2025.100128","DOIUrl":"10.1016/j.nbscr.2025.100128","url":null,"abstract":"","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100128"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184331","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":"Local versus global sleep organization and the quest to determine sleep function","authors":"Hans P.A. Van Dongen","doi":"10.1016/j.nbscr.2025.100117","DOIUrl":"10.1016/j.nbscr.2025.100117","url":null,"abstract":"<div><div>The research of JM Krueger and colleagues, focusing on sleep organization as a means to elucidate sleep function, led to critical insights as to why we sleep. Krueger posited that, fundamentally, sleep occurs locally at the level of neuronal/glial assemblies (small networks of neurons and glia) and that the expression of sleep in these assemblies is dependent on their prior use. Neuronal/glial assemblies serve as units of information processing, which consumes energy and increases entropy so that the energy available for further information processing is use-dependently depleted. According to the laws of physics, when energy drops to a lower bound relative to entropy, information processing ceases – which results in local quiescence and locally reduced consciousness and manifests as <em>use-dependent local sleep</em>. The physics-based nature of local sleep implies that it is inevitable, has neither function nor purpose, and is by itself not subject to biology-based evolutionary shaping. But uncontrolled local sleep compromises vigilance and is a threat to safety, which needs to be addressed to ensure survival. This can be accomplished by preemptively regulating sleep at a more global level and in a way that is adapted to the organism's temporal, environmental and ecological niche. Such global sleep allows for energy resupply (through biological processes not unique to sleep) across many neuronal/glial assemblies simultaneously while the organism is relatively safe. Thus, <em>global sleep regulation</em> could be the biology-based adaptation to the physics-based problem of use-dependent local sleep intrusions into wakefulness. Global sleep precludes niche exploitation and thus comes at an opportunity cost – but, unlike local sleep, the regulation of global sleep is subject to evolutionary shaping and amenable to species-specific optimization. Furthermore, a variety of ancillary functions may be served during global sleep to retroactively address biological needs that arose from prior wakefulness. However, serving these functions may be merely opportunistic, as the temporal dynamics of global sleep regulation appear to be proactive rather than retroactive, prioritizing alignment of global sleep and wake timing with the organism's ecological niche. Regardless, the costs of use-dependent local sleep and the management thereof through global sleep regulation are likely to be outweighed by the evolutionary benefit of the presumed source of the local sleep problem – that is, information processing capability, or cognition. In essence, therefore, sleep may just be the unavoidable, but worthwhile, price we pay for cognition.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184337","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":"Modulation of adult hippocampal neurogenesis by interleukin 1 signaling","authors":"Maria I. Smirnova ,&nbsp;Ning Quan","doi":"10.1016/j.nbscr.2025.100123","DOIUrl":"10.1016/j.nbscr.2025.100123","url":null,"abstract":"<div><div>Adult hippocampal neurogenesis (AHN) plays a critical role in cognition and emotional regulation. Recent studies have linked compromised AHN to numerous neurological and psychological disorders. The actions of the inflammatory cytokine interleukin-1 (IL-1) have been found to suppress AHN and antagonism of IL-1 signaling has been advocated as a therapeutic strategy for the treatment of neurodegenerative diseases and affective disorders. On the other hand, work from Jim Krueger's group revealed the physiological function of IL-1 in brain homeostasis, indicating the potential downside of IL-1 blockade. Current literature also shows AHN participates in normal functions of the brain in parallel to IL-1. This mini-review analyzes how IL-1 might positively or negatively modulate AHN and the implications of the relationship between IL-1 and AHN on health and disease. Specifically, we will highlight the parallels between IL-1 signaling and AHN in physiological and disease states. We propose that IL-1 signaling modulates AHN in a context-dependent manner; whereas its elevated signaling impairs neurogenesis and contributes to neurological and psychiatric disorders, its physiological role suggests potential therapeutic benefits of IL-1 antagonism must consider the preservation of the beneficial actions of IL-1.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100123"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184339","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":"Effect of chronic sleep restriction on ethanol preference and cortical structural plasticity","authors":"Fernando Bravo-González ,&nbsp;Mario Eduardo Acosta-Hernández ,&nbsp;Hiram Tendilla-Beltrán ,&nbsp;Gonzalo Flores ,&nbsp;Fabio García-García","doi":"10.1016/j.nbscr.2025.100126","DOIUrl":"10.1016/j.nbscr.2025.100126","url":null,"abstract":"<div><div>Sleep loss is associated with a potential risk of using drugs such as cocaine, methamphetamines, and alcohol. Recently, our group showed that chronic sleep restriction (CSR) for 7 days/4 h induces a significant increase in ethanol intake and delta FosB immunoreactivity in the rat's prefrontal cortex. However, whether CSR promotes changes in structural plasticity that explain ethanol consumption is unknown. Therefore, the present study aimed to determine if CSR induces changes in the dendritic length, branching of the dendritic tree, and spine morphology of the pyramidal neurons from the prelimbic cortex and whether these structural changes are associated with ethanol consumption. For this purpose, adult male Wistar rats were divided into four experimental groups: control, CSR for 7 days/4 h daily, CSR + ethanol exposure, and ethanol exposure. The two-bottle free-choice paradigm was used to measure ethanol intake, and the gentle handling method was used for CSR. At the end of the experiment, the rats were euthanized, and their brains were dissected and processed by Golgi-Cox staining. Sholl analysis was used to characterize structural plasticity. Results show that CSR induced an increase in the ethanol index preference. In addition, ethanol intake and ethanol + CSR increased the total dendritic length, dendritic tree branching, and mushroom spines in prelimbic cortex neurons. In conclusion, changes in structural plasticity associated with CSR and continuous access to ethanol may translate into neuroadaptive changes that favor drug preference and subsequently reinforce addictive behavior.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100126"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184340","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":"Impact of domestic white LED light on cognitive functions and amelioration of blue light blocking lens (BBL) on healthy adults","authors":"Mousumi Ghosh ,&nbsp;Hari Prakash Palaniswamy ,&nbsp;Nishitha. G ,&nbsp;Stelyna Joylin ,&nbsp;Shwetha. T.S ,&nbsp;M. Sanjana ,&nbsp;R.P. Radhika ,&nbsp;Nagarajan Theruveethi","doi":"10.1016/j.nbscr.2025.100119","DOIUrl":"10.1016/j.nbscr.2025.100119","url":null,"abstract":"<div><div>White light-emitting diodes <strong>(</strong>WLEDs) can affect cognition and working memory. Blue light-blocking lenses (BBL) may help alleviate this. We aim to study the relationship between WLED and the ameliorative effect of BBL. We included 15 healthy participants based on the PSQI and Mini-Cog™ screening. The eligible participants underwent a baseline recording of event-related potential (ERP) of P300 using electroencephalography (EEG) while performing a 2-back task, followed by exposure to WLED (600 lux) that was given (45° with 80 cm apart from the participant's eye plane) for 30 min. A similar protocol was maintained when BBL was worn with WLED exposure. The participants' mean PSQI and Mini-Cog™ scores (n = 15) were 3 and 5, respectively. The behavioral functioning of participants using a 2-back task revealed enhancement in working memory cognition by fastening the response time (ms) from base to post-WLED to post-WLED + BBL (p &lt; 0.001). Still, no significant difference (p &gt; 0.05) in accuracy (%) was observed. The learning effect in the control group using a 2-back task revealed no statistically significant difference (p &gt; 0.05) in both accuracy (%) and response time (ms). Additionally, no significant change (p &gt; 0.05) was found within the three light groups in latency (ms) and amplitude (μV) at the P300 region of ERP in the prefrontal cortex. The existing results found that domestic WLED exposure significantly leads to a faster response time in working memory performance in the prefrontal cortex, thus remaining alert. BBL is not protective in the nonvisual senses when exposed to WLED for 30 min.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100119"},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143869672","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":"Multiple oscillators underlie circadian food anticipation in mice","authors":"David E. Ehichioya ,&nbsp;Ishrat Masud ,&nbsp;S.K. Tahajjul Taufique ,&nbsp;Melody Shen ,&nbsp;Sofia Farah ,&nbsp;Shin Yamazaki","doi":"10.1016/j.nbscr.2025.100116","DOIUrl":"10.1016/j.nbscr.2025.100116","url":null,"abstract":"<div><div>Circadian pacemakers orchestrate behavioral and physiological rhythms, enabling organisms to anticipate daily reoccurring environmental events such as light and dark, temperature changes, and food availability. When nocturnal rodents are subjected to time-restricted feeding during the day, they typically display food anticipatory activity several hours before mealtime. Upon releasing mice to ad libitum feeding, this anticipatory activity is abolished immediately but, following food deprivation, reappears at approximately the same time. However, the mechanism by which rodents retain this time memory of food availability during ad libitum feeding has remained elusive. We utilized the open-source Feeding Experimentation Device 3 (FED3) to measure food-seeking nose-poking behavior. We programmed the FED3 to dispense a pellet by a single left nose-poke, but not by right poke. During daytime restricted feeding, mice exhibited strong anticipatory nose-poking a few hours prior to the daytime meal in both rewarded left and unrewarded right pokes. In addition, mice also exhibited elevation of both rewarded and unrewarded pokes at night, coinciding with mice's previous habitual feeding time. Following ad libitum feeding, rewarded daytime nose-poking gradually moved back to habitual nighttime. However, following food deprivation, anticipatory poking immediately reappeared during the day and night, coinciding with the times of previous daytime restricted feeding and nighttime habitual feeding. Under ad libitum feeding, db/db mice didn't exhibit a clear daily rhythm in food intake. However, these mice exhibited robust food anticipation in both nose-pokes and activity during daytime restricted feeding. Following release back to ad libitum feeding, db/db mice poked sporadically during the day and night, and following food deprivation, anticipation promptly reappeared. These data suggest that there are at least two oscillators underlying food anticipation: one oscillator with a phase that changes according to food availability, and another oscillator with a phase unaffected by feeding conditions. In db/db mice, the first oscillator is likely impaired, and the second oscillator is unaffected.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of restless legs syndrome and obesity: A sub-population of the MASHAD cohort study","authors":"Azam Vafaei ,&nbsp;Fatemeh Khorashadizadeh ,&nbsp;Maryam Saberi-Karimian ,&nbsp;Sara Saffar Soflaei ,&nbsp;Mahnaz Amini ,&nbsp;Abolfazl Rashid ,&nbsp;Sara Yousefian ,&nbsp;Gordon A. Ferns ,&nbsp;Habibollah Esmaily ,&nbsp;Majid Ghayour-Mobarhan ,&nbsp;Reza Salaran ,&nbsp;Fatemeh Taherian","doi":"10.1016/j.nbscr.2025.100113","DOIUrl":"10.1016/j.nbscr.2025.100113","url":null,"abstract":"<div><h3>Introduction</h3><div>Restless Legs Syndrome (RLS), as a relatively unknown sleep disorder, often associated with obesity. The purpose of this study was to examine the relationship between RLS and different definitions of obesity within the Mashhad stroke and heart atherosclerotic disorder (MASHAD) cohort study population.</div></div><div><h3>Methods</h3><div>A total of 1006 subjects, with an average age of 57 (51.75–63.00) years old, were randomly selected from the MASHAD cohort study phase II. This sample included 449 males and 557 females, who were contacted by phone to inquire about RLS. Anthropometric measurements such as weight, height, waist circumference (WC), and hip circumference (HC) were taken. Central obesity was defined as a WC &gt; 90 cm for men and &gt;85 cm for women, as well as a waist-to-hip ratio (WHR) greater than 0.90 for men and 0.85 for women. Statistical analyses were conducted using R version 4.3.2 for Windows, with a significance level set at a two-sided P-value&lt;0.05. Chi-squared and Fisher's exact tests were used to compare the categorical variables between two study groups. Logistic models applied to evaluate the association between RLS and BMI while adjusting for age effects.</div></div><div><h3>Results</h3><div>The study found a significant relationship between RLS and employment status (p-value = 0.04), marital status (p-value = 0.05), and BMI (p-value&lt;0.001). The results showed that in the total population, the OR of RLS in subjects having BMI&gt;30 kg/m² increased to 1.50(1.10–2.03) after adjusting for confounding factors (p-value&lt;0.01). A BMI&gt;30 kg/m² increased odds of RLS by 1.72 times in males (95%CI: 1.03–2.84, p-value&lt;0.05), however this association was diminished after adjustment (OR = 1.20, 95%CI: 0.64–2.17). There was no significant association between BMI and RLS in females. Moreover, there was no significant association between RLS and obesity based on WC and WHR in fully adjusted model respectively.</div></div><div><h3>Conclusion</h3><div>There was a significant association between BMI and RLS. A BMI&gt;30 kg/m² increased the odds of RLS by 1.50 times in the study population.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100113"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}