In-home validation of wrist- and waist-worn devices against portable electroencephalography for sleep assessment in community-dwelling older adults.

Polysomnography parameters in typically development and neuropsychiatric children: A systematic review and meta-analysis.

This study examined the effects of intensified endurance training on nocturnal skin temperature and sleep variables in male long-distance runners. Fourteen runners completed two different 8-day training programs: one with intensified training (INT) and one with normal training (NOR). At night, proximal (chest) skin temperature was measured every 5 min. Sleep variables, including efficiency, total time, latency, and wake time after sleep onset (WASO), were assessed for 8 consecutive days. Running distance over 8 days was significantly higher in INT (209.2 ± 17.4 km) than in NOR (118.5 ± 31.2 km, p = 0.01). Maximum skin temperature was significantly higher (p = 0.045) throughout the night in INT, especially during the first 180 min after bedtime (p = 0.03). Delta (Δ) skin temperature (maximum - minimum) during sleep was higher in INT than in NOR (p = 0.004). Sleep latency was significantly longer in INT (8.4 ± 4.0 min) than in NOR (2.6 ± 1.9 min, p = 0.003). Eight consecutive days of intensified endurance training elevated nocturnal proximal skin temperature with increased sleep latency. These findings suggest that increased training volume may alter nocturnal thermoregulatory responses and delay sleep initiation without substantially impairing overall sleep quantity.

Sleep-wake disorders are common in numerous neurological and psychiatric conditions, yet current treatments often yield incomplete results. Given the subcortical nature of sleep regulation, intracranial stimulation, and particularly deep brain stimulation (DBS), emerges as a promising therapeutic strategy. This narrative review synthesizes preclinical and clinical evidence regarding the effects of DBS and DBS-like invasive stimulation across multiple brain regions implicated in sleep-wake (SW) control. Additionally, stimulation targeting non-SW related targets has also shown incidental effects on sleep and wakefulness. Evidence reveals target- and frequency-dependent effects on sleep architecture and arousal, with notable translational success in Parkinson's Disease and Obsessive-Compulsive Disorder. The discussion addresses three central questions: (1) Which brain areas modulate sleep and wakefulness when stimulated? (2) How do stimulation parameters influence these outcomes? (3) What are the challenges and limitations in moving toward sleep-wake-primary indications? Despite encouraging results, variability in reported measures and outcomes underscores the need for objective, standardized sleep measures (polysomnography) and advanced targeting. Overall, this review may assist clinicians in optimizing DBS parameters in patients experiencing sleep-wake disturbances and underscores the broader potential of invasive neuromodulation both as a therapeutic strategy and as a tool to better characterize sleep and wakefulness dynamics.

Research on sleep in bulimia nervosa (BN) is methodologically varied and yields inconsistent findings. This review synthesised BN-sleep studies and examined whether comorbid mood disorders contribute to sleep disturbance. PsycINFO, Medline (Ovid), and Scopus were searched for English or French quantitative studies comparing sleep health variables between individuals with diagnosed BN and healthy controls. Extracted data included study design, sample characteristics, sleep and BN measures, and key findings. Methodological quality was evaluated using a validated risk-of-bias tool. Of 1233 titles/abstracts and 39 full texts screened, 11 studies met inclusion criteria. Some studies using subjective measures reported greater sleep disturbance in individuals with BN, including poorer sleep quality, difficulty initiating or maintaining sleep, and increased daytime sleepiness, with moderate to large effect sizes (|d|=0.60-1.43). Objective findings were mixed: one actigraphy study reported later sleep onset and wake times in BN, while findings for sleep efficiency and rapid eye movement (REM) sleep parameters were inconsistent, and most polysomnography (PSG) variables showed no reliable group differences despite some large effect sizes (range: |d|=0.72-1.69). Sleep disturbances were reported in some BN samples with and without comorbid mood disorders, although the specific contribution of mood pathology remains unclear. Studies were generally small, cross-sectional, and dated. Some studies suggest elevated subjective sleep disturbances in individuals with BN, but findings remain heterogeneous and are limited by methodological variability and small sample sizes. Future studies are needed to better characterise sleep health in individuals with BN. The systematic review was registered with the International Prospective Register of Systematic Reviews (CRD42022354504).

ABSTRACT Ramadan intermittent fasting alters sleep–wake patterns, dietary intake, and daily routines, which may interact with circadian timing and fatigue to influence athletic performance. This study examined the effects of Ramadan fasting on sleep, dietary intake, cognitive performance, and anaerobic running performance across different times of day and fatigue states in elite karate athletes. Twelve elite male karate athletes completed a within-subject repeated-measures protocol before Ramadan, during the second week, and during the fourth week of Ramadan. Testing was conducted at 08:00, 17:00, and 22:00. Simple reaction time, multiple-choice reaction time, Stroop performance, and 5-m multiple shuttle run performance were assessed before and after a karate-specific aerobic fatigue protocol. Sleep and dietary intake were monitored throughout each period. Ramadan fasting significantly reduced total sleep time, sleep efficiency, total energy intake, carbohydrate intake, and fat intake, while increasing subjective sleepiness and fatigue. Cognitive and physical performance were significantly affected by Ramadan period, time of day, and fatigue state. The greatest deterioration occurred during the fourth week of Ramadan, particularly at 17:00, when both reaction-time performance and shuttle-run outcomes showed the largest impairments compared with pre-Ramadan values. Performance decrements were also observed at 22:00, whereas morning performance at 08:00 was relatively preserved. Exercise-induced fatigue further worsened cognitive and physical outcomes and attenuated normal time-of-day variation. These findings indicate that Ramadan intermittent fasting induces sleep disruption, dietary alterations, and time-of-day dependent impairments in elite karate athletes. The late afternoon, particularly 17:00 during the fourth week of Ramadan, appears to be the most vulnerable period for cognitive and physical performance deterioration, especially under fatigue. Training load, recovery strategies, sleep management, and nutritional timing should therefore be carefully adapted during Ramadan.

Sleep disturbances (SD) are not merely symptoms of posttraumatic stress disorder (PTSD), but also amplify and perpetuate all other PTSD phenotypes. Ginsenoside Rg1 is extensively applied in managing neuropsychiatric diseases. Nevertheless, its impact on PTSD‐like SD and mechanisms remain largely unknown. In this study, the PTSD model in mice was produced using single‐prolonged stress (SPS) and the improvement effect of ginsenoside Rg1 on PTSD‐like behavior in mice, especially the sleep–wake phase was detected. The potential targets and signaling pathways of ginsenoside Rg1 as an intervention for treatment of PTSD with sleep disturbances (PTSD‐SD) were predicted using bioinformatics analysis. Thereafter, in vivo experiments were further used to verify the results. Our data showed that 14 days after SPS, the sleep architecture of mice was significantly disturbed, while ginsenoside Rg1 could treat PTSD‐like SD in SPS mice. The results of bioinformatics analysis suggested that NLRP‐related pathways and apoptosis may be the key factors for ginsenoside Rg1 to treat PTSD‐like sleep disturbances. Meanwhile, animal experiments also showed that the NLRP3 inflammasome, oxidative stress and apoptosis‐related markers were abnormally expressed in the hippocampus of SPS mice, but the administration of ginsenoside Rg1 could counteract the dysregulated expression of the above proteins in SPS mice. Finally, the results of docking revealed that ginsenoside Rg1 had favorable binding affinity with verified targets including NF‐κB, NLRP3, ASC, GFAP, HO‐1, and cleaved caspase‐3. Collectively, ginsenoside Rg1 is effective to prevent PTSD‐like SD, likely by regulating systemic comprehensive responses.

ABSTRACTObjectiveAutonomic nervous system (ANS) dysfunction is implicated in sleep‐disordered breathing (SDB) and atrial fibrillation (AF); however, diurnal patterning of ANS function in SDB is unclear. We hypothesize diurnal variation of heart rate variability (HRV) in paroxysmal AF (PAF) in SDB and alteration by continuous positive airway pressure (CPAP).MethodData from the Sleep Apnea and Atrial Fibrillation Biomarkers and Electrophysiologic Atrial Triggers (SAFEBEAT) study including 7–24 days of electrocardiography (ECG), concomitant actigraphy and polysomnography at baseline and 3 months post‐CPAP initiation were analyzed. Linear mixed‐effects models were used to assess (1) SDB: apnea hypopnea index (AHI), hypoxia (%sleep time with SaO2 < 90% and nadir SaO2) and (2) diurnal average HRV in 2 domains: frequency domain (sympathovagal) with low‐frequency (LF) power (LFP), high‐frequency (HF) power (HFP), LF/HF ratio (LHR), and time domain with mean of normal R‐R interval (MNN), standard deviation of NN intervals (SDNN), Poincare plot standard deviation short‐term and long‐term variability (SD1, SD2) and effect of CPAP. All results were adjusted for age, sex, race, BMI, and use of antihypertensive, antiarrhythmic, and atrioventricular nodal blockade medications.ResultsIn 44 869 5‐min epochs from 109 participants with SDB and PAF, associations of AHI and LFP, nadir SaO2 with sympathovagal measures (LFP, LHR) and time domain measures (SDNN, SD2) were observed during wakefulness. Sleep–wake interactions were observed for multiple HRV measures, with associations generally more evident during wakefulness. From baseline to follow‐up after CPAP, wakefulness HRV measures showed an increase in MNN and decreases in SDNN, RMSSD, CV, SD1, and SD2. During sleep, MNN, SD2, and LHR increased.ConclusionsAutonomic measures exhibited diurnal variation in moderate–severe SDB and were influenced by CPAP. Association with SDB severity was more pronounced during wakefulness, providing key insights into likelihood of sustained chronobiologic electrophysiological remodeling.

BackgroundPostoperative insomnia is one of the common complaints caused by spinal metastatic cancer surgery. It affects patients’ functional recovery, greatly reduces their quality of life, and adversely impacts disease prognosis. Compared with traditional pharmacological treatments, acupuncture is an alternative therapy for postoperative insomnia. However, standardized, high-quality randomized controlled trials on electroacupuncture for postoperative insomnia in patients with spinal metastasis (SM) are scarce, and there is a lack of clear inclusion criteria for this specific population. Postoperative insomnia in patients with SM has distinct clinical characteristics compared with general cancer-related insomnia, necessitating targeted investigation.ObjectiveThis study aims to evaluate the efficacy and safety of electroacupuncture in the treatment of postoperative insomnia in patients with SM, and to provide high-level clinical evidence for the inclusion of electroacupuncture in the clinical management plan of postoperative insomnia in patients with SM.MethodsThis is a study protocol for a randomized controlled trial. We will randomly assign 196 patients with insomnia after spinal metastatic cancer surgery to the acupuncture group (n=98) or the control group (sham acupuncture group; n=98). All participants will be treated on the first day after surgery and receive 12 sessions in total (30 min per session, 3 sessions per wk for 4 weeks). The primary outcome is the change in Pittsburgh Sleep Quality Index score from baseline to post treatment (wk 4). The secondary outcomes include actigraphy records (sleep efficiency, number of sleep awakenings, total sleep time, sleep latency, and wake after sleep onset), Insomnia Severity Index, Spine Oncology Study Group Outcomes Questionnaire 2.0, and Patient Health Questionnaire-9. All results will adhere to the intention-to-treat principle and will be evaluated at baseline, posttreatment (wk 4), and follow-up (wk 12).ResultsThis study was funded in June 2023 (supported by the Project of Shanghai Municipal Health Commission, National Natural Science Foundation of China, etc). Recruitment will start in mid-2026 and end in December 2027. Data collection will be completed in October 2027, and data analysis is expected to be finished in December 2027. The results of this study are anticipated to be published in the first half of 2028.ConclusionsThis study is designed to rigorously assess the therapeutic value of electroacupuncture for postoperative insomnia in patients with SM. If proven effective, electroacupuncture is expected to become a safe and feasible alternative or complementary therapy for this population, reducing reliance on hypnotic drugs and improving patients’ quality of life and prognosis. The results will fill the gap in current clinical evidence for electroacupuncture in the treatment of spinal metastatic postoperative insomnia and provide a basis for the optimization of clinical treatment strategies.

ABSTRACTThe human brain exhibits inherent multistability, with Energy Landscape Analysis (ELA) providing effective frameworks for investigating this property through BOLD signals. However, traditional amplitude‐based approaches fundamentally neglect critical phase synchronization dynamics that mediate large‐scale neural coordination, while existing phase‐based methods like Leading Eigenvector Dynamic Analysis (LEiDA) lack thermodynamic formalism for state stability quantification. Here, we introduce Energy‐based Phase‐Locking State Analysis (EPLSA), a transformative computational framework that synergistically integrates instantaneous phase‐coupling dynamics with rigorous energy landscape principles, addressing fundamental limitations of conventional methodologies. Comprehensive validation across two independent neuroimaging datasets (HCP and Natural Sleep) demonstrated EPLSA's marked superiority over LEiDA and conventional ELA in terms of test–retest reliability, task‐specific brain state differentiation, and individual‐level classification performance. To demonstrate the physiological and clinical utility of the proposed method, sleep–wake analysis was performed to reveal EPLSA's enhanced sensitivity to consciousness state transitions, identifying decreased primary state occupancy and increased minor state prevalence during sleep, with significantly reduced direct transition probabilities. Furthermore, application to patients with Alzheimer's disease using the OASIS‐3 dataset identified shortened dwell time and occurrence frequency for the frontoparietal control network‐default mode network (FPCN‐DMN) co‐activation state, and prolonged dwell time and occurrence frequency for the visual network‐limbic network (VIS‐LMN) co‐activation state, with these metrics significantly correlating with cognitive impairment. By unifying phase‐coupling and thermodynamic principles, EPLSA provides novel insights into neurodynamic mechanisms across cognitive tasks, consciousness states, and neurodegenerative conditions, offering a transformative analytical tool for investigating brain function in health and disease with particular promise for early detection and monitoring of neurological disorders.

A meta-analysis was used to explore the effects of single-component sleep restriction therapy (SRT) on insomnia in adults. PubMed, EMBASE, OVID, Scopus, Cochrane Library, and the Web of Science databases were searched until 31 July 2024. Literature quality evaluation was performed using Cochrane Collaboration's tool, and meta-analysis was performed using RevMan 5.4 software. For variables with low heterogeneity, fixed-effect models were employed to pool effect sizes; otherwise, the random effect model was used. Nine studies with 1239 participants were included. At post-treatment, fixed-effects models revealed significant benefits of SRT versus control for insomnia severity (points), sleep onset latency (minutes) measured by sleep diary or actigraphy and sleep quality measured by sleep diary. Random-effects models revealed significant benefits of SRT versus control for sleep efficiency (percentage) measured by sleep diary and wake time after sleep onset (minutes) measured by sleep diary. Besides, fixed-effects models revealed that, compared to control, as an expected consequence of the treatment mechanism, SRT led to a significant reduction in total sleep time (minutes). Long-term follow-up data indicated sustained SRT effects on insomnia severity, sleep efficiency and wake time after sleep onset, but not on sleep onset latency. Our results confirm the effectiveness of SRT on insomnia in adults. However, the long-term effects of SRT are not consistent, and further studies are needed in the future.

Clinical approaches to hypersomnolence complaints in psychiatry: A narrative review.

Perinatal arterial ischemic stroke - Is amplitude integrated EEG a helpful tool for the clinician?

BackgroundChild abuse and low parental affection are established risk factors for higher adulthood panic disorder (PD) severity, but their plausible sleep mediators are under-investigated. We thus examined how actigraphy indices mediated the links between child parental abuse and affection deficits to adulthood PD severity.MethodsCommunity-dwelling adult participants (N = 1,054) completed a series of self-reports on child parental abuse and affection at Wave 1. An eight-day actigraphy protocol was conducted at Wave 2, 9 years later. Telephone-administered clinical interviews assessing PD symptoms were conducted in W1 and Wave 3, separated by 18 years. A series of bias-corrected, bootstrapped causal mediation analyses was performed.ResultsPaternal, but not maternal abuse, predicted higher rest- and sleep-stage actigraphy markers after 9 years (βs = 0.263–469.79, p < .001), comprising more activity counts, longer wake time, higher wake time percentage, and wake bouts. These markers, thereby, mediated the trajectory from paternal abuse to higher PD severity (average causal mediation effects (ACMEs): βs = 0.003–0.020, 95% CIs excluding zero, p < .001). Likewise, paternal affection deficits predicted greater disturbances in rest- and sleep-stage actigraphy (all p < .05), thereby mediating the link to greater PD severity (ACMEs: βs = 0.001–0.002, p ≤ .04). Neither maternal abuse nor affection was a significant mediator.DiscussionThese outcomes aligned with, but do not verify, a causal mediation argument wherein actigraphy-derived nocturnal sleep–wake disturbances partially accounted for the trajectory from adverse paternal caregiving encounters to adulthood PD severity. Strategically targeting sleep disturbances may reflect a viable intervention approach for persons with past child paternal abuse learning histories.

Alzheimer's disease (AD) is associated with behavioral and physical manifestations, such as sleep disturbances, which worsen the course of the disease and require effective management strategies. This review investigates non-pharmacological interventions available for the control of sleep disorders in patients with Alzheimer's disease. This is an integrative review, with searches carried out in the Public Medical Database, Science Direct, Scientific Electronic Library Online and Latin American and Caribbean Literature in Health Sciences, using the descriptors: "Alzheimer Disease", "Sleep Wake Disorders", "Sleep Disorders", and "Therapeutics". Original studies evaluating non-pharmacological treatments for sleep disorders in patients with AD and using specific instruments to assess improvement in sleep disorders were included. The non-pharmacological interventions evaluated included bright light therapy, morning light exposure, personalized lighting intervention, blue-enriched white light exposure, transcranial magnetic stimulation, acupressure, multimodal exercise program, aromatic oil bath salts, light visor phototherapy, transcutaneous electrical nerve stimulation and deep brain stimulation. Additionally, one article investigated the combination of bright light exposure with walking, as well as the isolated effects of each intervention. Non-pharmacological interventions for managing sleep disorders in patients with AD have shown promising strategies, including approaches such as light therapy, physical stimulation techniques, and acupressure, with results indicating potential benefits in improving sleep quality and mitigating behavioral and cognitive symptoms associated with the disease. However, current evidence highlights the need for future studies with more rigorous methodologies, larger population samples, and long-term follow-up to consolidate the efficacy and applicability of these interventions in clinical practice.

Sleep disturbances and poor sleep quality are growing public health concerns, adversely affecting both physical and mental health. While exogenous melatonin supplements are used to manage the condition, there is limited evidence available on the efficacy of sustained-release (SR) melatonin formulations. This multicenter, randomized, double-blind, placebo-controlled clinical trial evaluated the efficacy and safety of melatonin-SR capsules (2 mg) in healthy adults with poor sleep quality. Participants aged 30-60 years with poor sleep quality received melatonin-SR (2 mg) or a placebo capsule at night for 28 days. Changes from baseline to day 28 in polysomnography (PSG)-derived sleep parameters, Pittsburgh Sleep Quality Index (PSQI), WHO-5 Well-Being Index, sleep diary parameters, and safety profile were evaluated. Of 62 enrolled participants, 59 (melatonin-SR, n = 28; placebo, n = 31) completed the study. Compared with placebo, melatonin-SR supplementation resulted in significant improvements at day 28 in PSG-derived sleep efficiency (change from baseline: 3.49 for melatonin-SR vs. -6.30% for placebo; p = 0.001) and total sleep time (change from baseline: 23.83 for melatonin-SR vs. -39.25 min for placebo; p = 0.001), along with significant reductions in sleep onset latency (change from baseline: -10.28 for melatonin-SR vs. 16.70 min for placebo; p = 0.031) and wake after sleep onset (change from baseline: -14.92 for melatonin-SR vs. 24.71 min for placebo; p = 0.001). Melatonin-SR supplementation demonstrated a large treatment effect for the improvement in sleep efficiency compared with placebo (Cohen's d = 0.9). A significant reduction in PSQI global scores was observed in the melatonin-SR group from day 07 onwards (change from baseline on day 07: -2.21 vs. -0.23; day 14: -4.86 vs. -0.65; and day 28: -5.61 vs. -0.65 for melatonin-SR and placebo, respectively; p = 0.001). Improvement in subjective psychological well-being was significant from day 14 onwards (change from baseline on day 14: 9.86 vs. 0.77; and day 28: 13.29 vs. 0.77 for melatonin-SR and placebo, respectively; p = 0.001). A significant improvement in subjective sleep parameters at day 28 (p < 0.05) was observed. Reported adverse events in both groups were mild and transient in nature. Supplementation with melatonin-SR 2 mg capsule at night for 28 days was found to be effective and safe in improving objective and subjective sleep quality outcomes and overall well-being in the trial population.

Background:Major depressive disorder (MDD) is a complex psychiatric condition characterized by affective, cognitive, and somatic symptoms. Disturbances in sleep and cognition are common yet underexplored features of MDD. Orexin, a hypothalamic neuropeptide, plays key roles in arousal, sleep–wake regulation, and cognition. This was a prospective, observational study with longitudinal follow-up investigating the correlation between serum orexin-A levels and depression symptom severity, sleep quality, and cognitive status, as assessed with standard psychometric tools.Methods:A total of 113 patients with MDD and 60 age- and sex-matched healthy controls were assessed in this study. Patients were followed up after 6–12 weeks of antidepressant therapy. Symptom severity, sleep quality, and cognitive status were assessed using the Montgomery–Åsberg Depression Rating Scale (MADRS), the Pittsburgh Sleep Quality Index (PSQI), and the Montreal Cognitive Assessment (MoCA), respectively. Serum orexin-A was quantified using an enzyme-linked immunosorbent assay (ELISA). The correlation between changes in serum orexin-A levels and clinical scale scores was assessed.Results:The median (Q1–Q3) serum orexin levels in patients and healthy controls were 192.6 (183.2–209.3) pg/mL and 207.4 (203.8–218.7) pg/mL, respectively, with a statistically significant difference (p < .001). Serum orexin-A levels in the patient group at baseline and follow-up were not statistically significant. Changes in various score components of the questionnaires were statistically significant. However, serum orexin-A levels were correlated only with the apparent sadness component of MADRS. No correlation was observed between orexin-A levels and PSQI or MoCA questionnaire components.Conclusions:Serum orexin-A showed potential as a biomarker for MDD, exhibiting correlation with a MADRS score component. However, no correlation was observed with sleep quality and cognitive status, necessitating validation in larger cohorts.

Background: Sleep disturbances are common in adults with attention-deficit/hyperactivity disorder (ADHD) and often include problems such as insomnia and circadian rhythm disturbances, which may negatively affect cognitive functioning and daily performance. However, their clinical characteristics and underlying mechanisms in adult ADHD remain incompletely understood. Aim: This narrative review synthesizes current evidence on sleep disturbances in adults with ADHD, focusing on prevalence, clinical characteristics, types of sleep disorders, mechanisms, and clinical implications. Materials and Methods: ​​This narrative review was based on the analysis of published scientific literature retrieved from online databases related to attention-deficit/hyperactivity disorder (ADHD) and sleep. Relevant publications were selected based on their relevance to the topic, with a focus on studies involving adult populations. Most of the included studies were published between 2015 and 2026, with earlier key publications included for background context. Various types of studies were considered, including reviews, clinical studies, and theoretical papers. The findings were synthesized qualitatively. Results: Approximately 60% of adults with ADHD screen positive for sleep disorders, primarily insomnia and delayed sleep–wake phase disorder. Underlying mechanisms are multifactorial, involving circadian dysregulation, neurobiological, and behavioral factors. These issues are also associated with psychiatric comorbidities and impairments in executive functioning. Conclusions: Sleep disturbances represent a clinically relevant aspect of adult ADHD. Their heterogeneity and complex mechanisms should be considered in clinical practice. Further research is needed to clarify their characteristics and the role of sleep-focused interventions.

BackgroundSleep disturbances elevate brain amyloid-beta (Aβ) levels and represent a modifiable risk factor for Alzheimer’s disease (AD). The orexin/hypocretin system regulates sleep–wake behavior and has emerged as a therapeutic target in AD; however, the effects of FDA-approved dual orexin receptor antagonists (DORAs) on amyloid pathology remain unclear. We compared lemborexant, an FDA-approved DORA, to doxepin, an antihistaminergic sleep medication, on amyloid pathology and microglial responses in PSAPP mice.MethodsPSAPP mice received lemborexant (10 or 30 mg/kg/day), doxepin (35 mg/kg/day), or vehicle for 6 weeks beginning prior to plaque onset or 4 weeks after established pathology. Sleep was assessed by piezoelectric monitoring and EEG/EMG polysomnography. Amyloid pathology and microglial responses were quantified by immunohistochemistry, confocal microscopy, and single-cell RNA sequencing. Microglial depletion was induced with the CSF1R inhibitor PLX3397.ResultsLemborexant enhanced sleep quality with less active-phase sedation than doxepin. Both drugs reduced initial diffuse plaque deposition, but only lemborexant prevented fibrillar plaque accumulation in young mice and slowed plaque growth in older mice. Lemborexant increased peri-plaque microglial CD68 expression and enhanced Aβ phagocytosis in vivo. Single-cell transcriptomics revealed a shift toward activated, DAM-like microglial states with upregulation of phagocytic genes without broad inflammatory induction. Microglial depletion abolished lemborexant’s anti-amyloid effects.ConclusionsLemborexant mitigates amyloid pathology by augmenting microglial phagocytic function, positioning DORAs as promising therapeutics that couple sleep promotion with beneficial microglial modulation.Supplementary informationThe online version contains supplementary material available at 10.1186/s13024-026-00948-y.

To examine the cross-sectional associations between objectively assessed physical activity and sedentary time, and both objectively and subjectively assessed sleep parameters (e.g., duration and quality) among Australian adolescents, including weekdays and weekends. Baseline data from the TransformUs Secondary effectiveness trial involved 193 adolescents (mean age 14.8 years) from Victoria, Australia. Participants self-reported bedtime and wake-up times on school nights and weekends, as well as sleep quality using the Adolescent Sleep Wake Scale. The wrist-worn ActiGraph GT9X was used to collect 24-hour activity data for over 1 week (minimum of 10h, at least 3 days) to assess moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), sedentary time, and sleep parameters, including total sleep time (TST), sleep efficiency, sleep latency, and wake after sleep onset (WASO). Linear regression models examined associations between physical activity, sedentary time, and sleep parameters. Sedentary time was inversely associated with self-reported sleep quality, and with objectively assessed weekday sleep duration and TST. No significant associations were observed between LPA, MVPA, and sleep parameters. These findings highlight the detrimental link between higher sedentary time and poor sleep quality and duration among adolescents, reinforcing the need to reduce sedentary behavior as a key intervention strategy for improving sleep health. Future prospective studies are needed to better understand temporal associations and the types of behaviour adolescents are engaging in when they are sedentary.