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The sleep homeostatic process in adults is moderately stable over time and unique to an individual. Work in transgenic mice has suggested a role of genes in sleep homeostasis. The current study quantified the genetic contribution to sleep homeostasis in adolescence. We use slow wave energy (SWE) as a metric for sleep pressure dissipation during sleep. This measure reflects both sleep intensity and duration. High‐density (58 derivations) sleep electroencephalogram (EEG) was recorded in 14 monozygotic and 12 dizygotic adolescent twin pairs (mean age = 13.2 years; standard deviation [SD] = 1.1; 20 females). SWE at the end of sleep was quantified as the cumulative delta power (1–4.6 Hz) over the night. We also examined the time constant of the decay and the level of slow wave activity (SWA) at the beginning of the sleep episode. Structural equation modelling was used to quantify the amount of variance in SWE and the dissipation of sleep pressure due to genes. We found that most (mean = 76% across EEG derivations) of the variance in SWE was due to genes. In contrast, genes had a small (mean = 33%) influence on the rate of dissipation of sleep pressure, and this measure was largely (mean = 67%) driven by environmental factors unique to each twin. Our results show that the amount of dissipated sleep pressure is largely under genetic control; however, the rate of sleep pressure dissipation is largely due to unique environmental factors. Our findings are in line with research in animals and suggest that the heritability of the rate of sleep pressure dissipation is limited. [ABSTRACT FROM AUTHOR]

Background: Cytokines, known for their pro- and anti-inflammatory roles, are also key regulators of sleep–wake cycles. Classical pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), are associated with increased sleep, particularly slow-wave sleep (SWS), while anti-inflammatory cytokines, like interleukin-10 (IL-10), generally reduce sleep duration. Given the essential role of sleep in memory consolidation, this study aimed to investigate whether interleukin-12 (IL-12), a pro-inflammatory cytokine, could increase sleep duration following a memory acquisition task and subsequently improve memory performance. Male Swiss mice were surgically implanted with electrodes for electrocorticogram (ECoG) and electromyogram (EMG) recordings to track their sleep–wake cycles. After a recovery period, baseline sleep–wake activity was recorded. The mice were then randomly assigned to two groups and treated with either IL-12 (0.5 µg, i.p.) or a phosphate-buffered saline (PBS, i.p.) control, administered immediately before the multiple-trial inhibitory avoidance (MTIA) task, a behavioral test used to assess memory performance. Following the memory acquisition session, sleep–wake activity was immediately recorded for a continuous 24-h period. Results: Mice treated with IL-12 exhibited longer latency to cross into the dark compartment during the MTIA test, indicating improved memory retention compared to the control group. Interestingly, this improved performance was associated with prolonged wakefulness, particularly in the first three hours after task acquisition. Conclusion: The study shows that IL-12 can improve memory retention through prolonged wake episodes rather than increased sleep. This finding challenges the conventional understanding that sleep is the primary state for memory consolidation, suggesting that under specific conditions, wakefulness may also play a key role in supporting memory processes. Further research is needed to explore the underlying mechanisms of IL-12's cognitive effects. [ABSTRACT FROM AUTHOR]

Summary The transition from non‐rapid eye movement (NREM) to rapid eye movement (REM) sleep is considered a transitional or intermediate stage (IS), characterised by high amplitude spindles in the frontal cortex and theta activity in the occipital cortex. Early reports in rats showed an IS lasting from 1 to 5 s, but recent studies suggested a longer duration of this stage of up to 20 s. To further characterise the IS, we analysed its spectral characteristics on electrocorticogram (ECoG) recordings of the olfactory bulb (OB), primary motor (M1), primary somatosensory (S1), and secondary visual cortex (V2) in 12 Wistar male adult rats. By comparing the IS with consolidated NREM/REM epochs, our results reveal that the IS has specific power spectral patterns that fall out of the NREM and REM sleep state power distribution. Specifically, the main findings were that sigma (11–16 Hz) power in OB, M1, S1, and V2 increased during the IS compared with NREM and REM sleep, which started first in the frontal part of the brain (OB −54 s, M1 −53 s) prior to the last spindle occurrence. The beta band (17–30 Hz) power showed a similar pattern to that of the sigma band, starting −54 s before the last spindle occurrence in the M1 cortex. Notably, sigma infraslow coupling (~0.02 Hz) increased during the IS but occurred at a slower frequency (~0.01 Hz) compared with NREM sleep. Thus, we argue that the NREM to REM transition contains its own local spectral profile, in accordance with previous reports, and is more extended than described previously. [ABSTRACT FROM AUTHOR]

Sleep associated memory consolidation and reactivation play an important role in language acquisition and learning of new words. However, it is unclear to what extent properties of word learning difficulty impact sleep associated memory reactivation. To address this gap, we investigated in 22 young healthy adults the effectiveness of auditory targeted memory reactivation (TMR) during non-rapid eye movement sleep of artificial words with easy and difficult to learn phonotactical properties. Here, we found that TMR of the easy words improved their overnight memory performance, whereas TMR of the difficult words had no effect. By comparing EEG activities after TMR presentations, we found an increase in slow wave density independent of word difficulty, whereas the spindle-band power nested during the slow wave up-states – as an assumed underlying activity of memory reactivation – was significantly higher in the easy/effective compared to the difficult/ineffective condition. Our findings indicate that word learning difficulty by phonotactics impacts the effectiveness of TMR and further emphasize the critical role of prior encoding depth in sleep associated memory reactivation. [ABSTRACT FROM AUTHOR]

Objective: We aimed to investigate sleep in children with drug‐resistant epilepsy (DRE), including developmental and epileptic encephalopathies (DEEs). Next, we examined differences in sleep macrostructure and microstructure and questionnaire outcomes between children with well‐controlled epilepsy (WCE) and children with DRE. Furthermore, we wanted to identify factors associated with poor sleep outcome in these children, as some factors might be targets to improve epilepsy and neurodevelopmental outcomes. Methods: A cross‐sectional study was conducted in children 4 to 18‐years‐old. Children without epilepsy, with WCE, and with DRE were included. Overnight electroencephalography (EEG), including chin electromyography and electrooculography, to allow sleep staging, was performed. Parents were asked to fill out a sleep questionnaire. Classical five‐stage sleep scoring was performed manually, spindles were automatically counted, and slow wave activity (SWA) in the first and last hour of slow wave sleep was calculated. Results: One hundred eighty‐two patients were included: 48 without epilepsy, 75 with WCE, and 59 with DRE. We found that children with DRE have significantly lower sleep efficiency (SE%), less time spent in rapid eye movement (REM) sleep, fewer sleep spindles, and a lower SWA decline over the night compared to children with WCE. Subjectively more severe sleep problems were reported by the caregivers and more daytime sleepiness was present in children with DRE. Least absolute shrinkage and selection operator (LASSO) regression showed that multifocal interictal epileptiform discharges (IEDs), benzodiazepine treatment, and longer duration of epilepsy were associated with lower SE% and lower REM sleep time. The presence of multifocal discharges and cerebral palsy was associated with fewer spindles. Benzodiazepine treatment, drug resistance, seizures during sleep, intellectual disability, and older age were associated with lower SWA decline. Significance: Both sleep macrostructure and microstructure are severely impacted in children with DRE, including those with DEEs. Epilepsy parameters play a distinct role in the disruption REM sleep, spindle count, and SWA decline. [ABSTRACT FROM AUTHOR]

Objective: To understand the etiological landscape and phenotypic differences between 2 developmental and epileptic encephalopathy (DEE) syndromes: DEE with spike–wave activation in sleep (DEE‐SWAS) and epileptic encephalopathy with spike–wave activation in sleep (EE‐SWAS). Methods: All patients fulfilled International League Against Epilepsy (ILAE) DEE‐SWAS or EE‐SWAS criteria with a Core cohort (n = 91) drawn from our Epilepsy Genetics research program, together with 10 etiologically solved patients referred by collaborators in the Expanded cohort (n = 101). Detailed phenotyping and analysis of molecular genetic results were performed. We compared the phenotypic features of individuals with DEE‐SWAS and EE‐SWAS. Brain‐specific gene co‐expression analysis was performed for D/EE‐SWAS genes. Results: We identified the etiology in 42/91 (46%) patients in our Core cohort, including 29/44 (66%) with DEE‐SWAS and 13/47 (28%) with EE‐SWAS. A genetic etiology was identified in 31/91 (34%). D/EE‐SWAS genes were highly co‐expressed in brain, highlighting the importance of channelopathies and transcriptional regulators. Structural etiologies were found in 12/91 (13%) individuals. We identified 10 novel D/EE‐SWAS genes with a range of functions: ATP1A2, CACNA1A, FOXP1, GRIN1, KCNMA1, KCNQ3, PPFIA3, PUF60, SETD1B, and ZBTB18, and 2 novel copy number variants, 17p11.2 duplication and 5q22 deletion. Although developmental regression patterns were similar in both syndromes, DEE‐SWAS was associated with a longer duration of epilepsy and poorer intellectual outcome than EE‐SWAS. Interpretation: DEE‐SWAS and EE‐SWAS have highly heterogeneous genetic and structural etiologies. Phenotypic analysis highlights valuable clinical differences between DEE‐SWAS and EE‐SWAS which inform clinical care and prognostic counseling. Our etiological findings pave the way for the development of precision therapies. ANN NEUROL 2024;96:932–943 [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a leading cause of mortality and morbidity among aging populations worldwide. Despite arduous research efforts, treatment options for this devastating neurodegenerative disease are limited. Sleep disturbances, through their link to changes in neural excitability and impaired clearance of interstitial abnormal protein aggregates, are a key risk factor for the development of AD. Research also suggests that the neuroprotective effects of sleep are particularly active during slow wave sleep. Given the strong link between sleep disturbance and AD, targeting sleep in the prodromal stages of AD, such as in mild cognitive impairment (MCI), represents a promising avenue for slowing the onset of AD-related cognitive decline. In efforts to improve sleep in older individuals, several pharmacologic approaches have been employed, but many pose safety risks, concern for worsening cognitive function, and fail to effectively target slow wave sleep. Trazodone, a safe and widely used drug in the older adult population, has shown promise in inducing slow wave sleep in older adults, but requires more rigorous research to understand its effects on sleep and cognition in the prodromal stages of AD. In this review, we present the rationale and study design for our randomized, double-bind, placebo-controlled, crossover trial (NCT05282550) investigating the effects of trazodone on sleep and cognition in 100 older adults with amnestic MCI and sleep complaints. [ABSTRACT FROM AUTHOR]

Binaural beats can entrain neural oscillations and modulate behavioral states. However, the effect of binaural beats, particularly those with slow frequencies (< 1 Hz), on sleep remains poorly understood. We hypothesized that 0.25-Hz beats can entrain neural oscillations and enhance slow-wave sleep by shortening its latency or increasing its duration. To investigate this, we included 12 healthy participants (six women; mean age, 25.4 ± 2.6 years) who underwent four 90-min afternoon nap sessions, comprising a sham condition (without acoustic stimulation) and three binaural-beat conditions (0, 0.25, or 1 Hz) with a 250-Hz carrier tone. The acoustic stimuli, delivered through earphones, were sustained throughout the 90-min nap period. Both N2- and N3- latencies were shorter in the 0.25-Hz binaural beats condition than in the sham condition. We observed no significant results regarding neural entrainment at slow frequencies, such as 0.25 and 1 Hz, and the modulation of sleep oscillations, including delta and sigma activity, by binaural beats. In conclusion, this study demonstrated the potential of binaural beats at slow frequencies, specifically 0.25 Hz, for inducing slow-wave sleep in generally healthy populations. [ABSTRACT FROM AUTHOR]

Introduction Methods Results Conclusion Sleep is crucial for physical and psychological health, and disturbances are closely linked to psychiatric disorders, making their management essential for improving treatment outcomes and preventing relapse. Although sleep disturbances are implicated in psychopathology of eating disorders, its role in anorexia nervosa (AN) remains unclear. This review aimed to characterise sleep in AN.A systematic search was conducted in four scientific databases, including papers from inception to 25 May 2024. A machine learning algorithm (ASReview) was utilised to screen titles and abstracts for eligibility. Sleep quantity, architecture, and quality were investigated. Meta‐analyses were conducted to investigate the difference between patients with AN and healthy controls (HC) in total sleep time (TST), wake after sleep onset (WASO), sleep onset latency (SOL), sleep efficiency, Sleep Stage 1, 2, slow wave sleep, rapid eye movement (REM) sleep and REM latency. Certainty of evidence was assessed using the GRADE approach.Out of 67 potentially eligible papers, 31 were included in this review, with 15 in the meta‐analyses. Statistically significant average mean differences were found for TST (−32.1 min [95% CI: −50.9, −13.4]), WASO (19.0 min [95% CI: −2.4, 40.3]), and sleep efficiency (−4.4% [95% CI: −7.9, −0.9]). Additionally, Sleep stage 1 was significantly increased (2.4% [95%‐CI: 0.05, 4.7]), while REM sleep was reduced (−2.1% [95%‐CI: −4.2, −0.02]). Subgroup analysis showed that TST and WASO did not improve significantly after weight restoration.Sleep in patients with AN is impaired, with lower TST and sleep efficiency, higher WASO, more time in stage 1 sleep, and less in REM. Weight restoration alone may not improve sleep. While more research is needed, substantial accompanying sleep disturbances in AN justifies addressing these in current treatment practice, also because of the chronic character of AN and importance of sleep for long term (mental) health. [ABSTRACT FROM AUTHOR]

The brain is a complex non-equilibrium system capable of expressing many different dynamics as well as the transitions between them. We hypothesized that the level of non-equilibrium can serve as a signature of a given brain state, which was quantified using the arrow of time (the level of irreversibility). Using this thermodynamic framework, the irreversibility of emergent cortical activity was quantified from local field potential recordings in male Lister-hooded rats at different anesthesia levels and during the sleep-wake cycle. This measure was carried out on five distinct brain states: slow-wave sleep, awake, deep anesthesia–slow waves, light anesthesia–slow waves, and microarousals. Low levels of irreversibility were associated with synchronous activity found both in deep anesthesia and slow-wave sleep states, suggesting that slow waves were the state closest to the thermodynamic equilibrium (maximum symmetry), thus requiring minimum energy. Higher levels of irreversibility were found when brain dynamics became more asynchronous, for example, in wakefulness. These changes were also reflected in the hierarchy of cortical dynamics across different cortical areas. The neural dynamics associated with different brain states were characterized by different degrees of irreversibility and hierarchy, also acting as markers of brain state transitions. This could open new routes to monitoring, controlling, and even changing brain states in health and disease. [ABSTRACT FROM AUTHOR]

Summary Deep sleep oscillations are proposed to be central in restoring brain function and to affect different aspects of motor performance such as facilitating the consolidation of motor sequences resulting in faster and more accurate sequence tapping. Yet, whether deep sleep modulates performance fatigability during fatiguing tasks remains unexplored. We investigated overnight changes in tapping speed and resistance against performance fatigability via a finger tapping task. During fast tapping, fatigability manifests as a reduction in speed (or “motor slowing”) which affects all tapping tasks, including motor sequences used to study motor memory formation. We further tested whether overnight changes in performance fatigability are influenced by enhancing deep sleep oscillations using auditory stimulation. We found an overnight increase in tapping speed alongside a reduction in performance fatigability and perceived workload. Auditory stimulation led to a global enhancement of slow waves and both slow and fast spindles during the stimulation window and a local increase in slow spindles in motor areas across the night. However, overnight performance improvements were not significantly modulated by auditory stimulation and changes in tapping speed or performance fatigability were not predicted by individual changes in deep sleep oscillations. Our findings demonstrate overnight changes in fatigability but revealed no evidence suggesting that this effect is causally linked to temporary augmentation of slow waves or sleep spindles. Our results are important for future studies using tapping tasks to test the relationship between sleep and motor memory consolidation, as overnight changes in objectively measured and subjectively perceived fatigue likely impact behavioural outcomes. [ABSTRACT FROM AUTHOR]

Slow waves are a distinguishing feature of non-rapid-eye-movement (NREM) sleep, an evolutionarily conserved process critical for brain function. Non-human studies suggest that the claustrum, a small subcortical nucleus, coordinates slow waves. We show that, in contrast to neurons from other brain regions, claustrum neurons in the human brain increase their spiking activity and track slow waves during NREM sleep, suggesting that the claustrum plays a role in coordinating human sleep architecture. The role of the human claustrum during slow wave sleep is unknown. Here the authors characterize the spiking activity of claustrum neurons in humans and demonstrate that claustrum neurons track slow waves during NREM sleep. [ABSTRACT FROM AUTHOR]

Memory consolidation involves repeated replay of new information by the hippocampus, which transfers memories to the neocortex for long-term storage. This occurs mainly during slow wave sleep, a phase characterized in the cortex by low cholinergic tone and low afferent input. High cholinergic tone has been shown to hamper memory consolidation, probably mediated by reduced network excitability (the ease of activity propagation in a network). We used cortical neuronal networks on multi electrode arrays to investigate whether low background input contributes to memory consolidation. Networks received focal electrical stimuli to memorize, with or without background afferent input (global optogenetic stimulation). Background stimulation hampered memory formation and consolidation, confirming the importance of low background input. Moreover, it lowered network excitability, similar to high cholinergic tone. These findings suggest that high network excitability is a critical feature of slow wave sleep that facilitates memory consolidation. [ABSTRACT FROM AUTHOR]

The article "Probing the embodiment of sleep functions: Insights from cardiac responses to word-induced relaxation during sleep" published in the Journal of Sleep Research explores the relationship between bodily functions, particularly cardiac activity, and cognitive functions during sleep. The study suggests that the presentation of relaxing words during non-rapid eye movement (NREM) sleep can lead to an increase in slow-wave sleep duration and subjective sleep quality. The research findings indicate that cardiac activity slows down in response to word-induced relaxation during NREM sleep, highlighting the importance of considering bodily signals in understanding sleep functions. The study aims to promote the investigation of cardiac responses in sleep research to provide a more comprehensive understanding of sleep functions and their modulation by sensory stimulation. [Extracted from the article]

Sharp wave‐ripple complexes (SPW‐Rs) are spontaneous oscillatory events that characterize hippocampal activity during resting periods and slow‐wave sleep. SPW‐Rs are related to memory consolidation – the process during which newly acquired memories are transformed into long‐lasting memory traces. To test the involvement of SPW‐Rs in this process, it is crucial to understand how SPW‐Rs originate and propagate throughout the hippocampus. SPW‐Rs can originate in CA3, and they typically spread from CA3 to CA1, but little is known about their formation within CA3. To investigate the generation and propagation of SPW‐Rs in CA3, we recorded from mouse hippocampal slices using multi‐electrode arrays and patch‐clamp electrodes. We characterized extracellular and intracellular correlates of SPW‐Rs and quantified their propagation along the pyramidal cell layer of CA3. We found that a hippocampal slice can be described by a speed and a direction of propagation of SPW‐Rs. The preferred propagation direction was from CA3c (the subfield closer to the dentate gyrus) toward CA3a (the subfield at the boundary to CA2). In patch‐clamp recordings from CA3 pyramidal neurons, propagation was estimated separately for excitatory and inhibitory currents associated with SPW‐Rs. We found that propagation speed and direction of excitatory and inhibitory currents were correlated. The magnitude of the speed of propagation of SPW‐Rs within CA3 was consistent with the speed of propagation of action potentials in axons of CA3 principal cells. Key points: Hippocampal sharp waves are considered important for memory consolidation; therefore, it is of interest to understand the mechanisms of their generation and propagation.Here, we used two different approaches to study the propagation of sharp waves in mouse CA3 in vitro: multi‐electrode arrays and multiple single‐cell recordings.We find a preferred direction of propagation of sharp waves from CA3c toward CA3a – both in the local field potential and in sharp wave‐associated excitatory and inhibitory synaptic activity.The speed of sharp wave propagation is consistent with the speed of action potential propagation along the axons of CA3 pyramidal neurons.These new insights into the dynamics of sharp waves in the CA3 network will inform future experiments and theoretical models of sharp‐wave generation mechanisms. [ABSTRACT FROM AUTHOR]

Exposure to infectious or non‐infectious immune activation during early development is a serious risk factor for long‐term behavioural dysfunctions. Mouse models of maternal immune activation (MIA) have increasingly been used to address neuronal and behavioural dysfunctions in response to prenatal infections. One commonly employed MIA model involves administering poly(I:C) (polyriboinosinic‐polyribocytdilic acid), a synthetic analogue of double‐stranded RNA, during gestation, which robustly induces an acute viral‐like inflammatory response. Using electroencephalography (EEG) and infrared (IR) activity recordings, we explored alterations in sleep/wake, circadian and locomotor activity patterns on the adult male offspring of poly(I:C)‐treated mothers. Our findings demonstrate that these offspring displayed reduced home cage activity during the (subjective) night under both light/dark or constant darkness conditions. In line with this finding, these mice exhibited an increase in non‐rapid eye movement (NREM) sleep duration as well as an increase in sleep spindles density. Following sleep deprivation, poly(I:C)‐exposed offspring extended NREM sleep duration and prolonged NREM sleep bouts during the dark phase as compared with non‐exposed mice. Additionally, these mice exhibited a significant alteration in NREM sleep EEG spectral power under heightened sleep pressure. Together, our study highlights the lasting effects of infection and/or immune activation during pregnancy on circadian activity and sleep/wake patterns in the offspring. [ABSTRACT FROM AUTHOR]

• Sigma activity is enhanced during the expiratory phase of respiration in non-rapid-eye-movement sleep. • Both slow and fast spindle events occurrence significantly increases during the middle part of the expiration phase. • Breathing exerts a lower biphasic effect on slow waves occurrence, which increases during respiration phase transitions. Coupling of sleep spindles with cortical slow waves and hippocampus sharp-waves ripples is crucial for sleep-related memory consolidation. Recent literature evidenced that nasal respiration modulates neural activity in large-scale brain networks. In rodents, this respiratory drive strongly varies according to vigilance states. Whether sleep oscillations are also respiration-modulated in humans remains open. In this work, we investigated the influence of breathing on sleep spindles during non-rapid-eye-movement sleep in humans. Full night polysomnography of twenty healthy participants were analysed. Spindles and slow waves were automatically detected during N2 and N3 stages. Spindle-related sigma power as well as spindle and slow wave events were analysed according to the respiratory phase. We found a significant coupling between both slow and fast spindles and the respiration cycle, with enhanced sigma activity and occurrence probability of spindles during the middle part of the expiration phase. A different coupling was observed for slow waves negative peaks which were rather distributed around the two respiration phase transitions. Our findings suggest that breathing cycle influences the dynamics of brain activity during non-rapid-eye-movement sleep. This coupling may enable sleep spindles to synchronize with other sleep oscillations and facilitate information transfer between distributed brain networks. [ABSTRACT FROM AUTHOR]

Background and Objectives: Developmental and epileptic encephalopathy refers to a group of conditions where patients experience abnormal development due to various causes as well as frequent epileptiform discharges that ultimately contribute, in an independent and additive fashion, to cognitive and linguistic impairments. The language and cognition outcome of these patients in adulthood has been understudied. This paper aims to present a scoping review of linguistic abilities in adults with developmental and epileptic encephalopathy to determine the extent to which language outcomes in adulthood and their relation to cognitive outcomes have been studied. Design: Two online databases were searched and the methodological framework by Arksey & O'Malley (2005) was adopted. Results: Out of the 27 selected studies, only 13 exclusively examined adults, 15 were group studies, 5 were case studies and 7 were case series. A total of 9 out of the 15 group studies provided individual results for adults. Twenty-two studies included a follow-up examination. Twenty-three studies addressed the relationship between language and cognition. The selected studies indicate the presence of language impairments, which are nevertheless differentially manifested in the syndromes under investigation, whereas individual variability is also reported. Aspects of cognition seem to correlate with linguistic abilities. Conclusions: In sum, despite variability in linguistic abilities, language deficits constitute a significant aspect of the clinical profile of many adults with developmental and epileptic encephalopathy, a finding that should be taken into account for the treatment protocols of these individuals. [ABSTRACT FROM AUTHOR]

Resting-state functional magnetic resonance imaging evolves through a repertoire of functional connectivity patterns which might reflect ongoing cognition, as well as the contents of conscious awareness. We investigated whether the dynamic exploration of these states can provide robust and generalizable markers for the state of consciousness in human participants, across loss of consciousness induced by general anaesthesia or slow wave sleep. By clustering transient states of functional connectivity, we demonstrated that brain activity during unconsciousness is dominated by a recurrent pattern primarily mediated by structural connectivity and with a reduced capacity to transition to other patterns. Our results provide evidence supporting the pronounced differences between conscious and unconscious brain states in terms of whole-brain dynamics; in particular, the maintenance of rich brain dynamics measured by entropy is a critical aspect of conscious awareness. Collectively, our results may have significant implications for our understanding of consciousness and the neural basis of human awareness, as well as for the discovery of robust signatures of consciousness that are generalizable among different brain conditions. Dynamical analysis of resting-state fMRI networks reveals a consistent increase in structure-function correlation and entropy decrease upon both general anesthesia-induced and deep sleep-induced loss of consciousness in humans. [ABSTRACT FROM AUTHOR]

Summary The active system consolidation theory assumes that sleep between encoding and retrieval promotes memory consolidation. In the present study, we cued new memories during slow‐wave (SWS) or rapid eye movements (REM) sleep stages by presenting an instrumental music stimuli that had been previously presented during a learning session. In a within‐subjects design, 18 participants slept for three nonconsecutive nights (cue during SWS, cue during REM, and no cue during control night) and were trained in a visuo‐spatial memory task. The administration of cue during SWS produced better memory accuracy in comparison with REM and the control condition. [ABSTRACT FROM AUTHOR]

Methods: We conducted a double-blind, randomised, placebo-controlled crossover trial with healthy older adults (65-79 years, n = 35). Participants first learned a word list and were then administered long-acting L-DOPA (or placebo) before a full night of sleep. Before sleeping, a proportion of the words were re-exposed using a recognition test to strengthen memory. L-DOPA was active during sleep and the practice-recognition test, but not during initial learning. Results: The single dose of L-DOPA increased total slow-wave sleep duration by approximately 11% compared to placebo, while also increasing spindle amplitudes around slow oscillation peaks and around 1-4 Hz NREM spectral power. However, behaviourally, L-DOPA worsened memory of words presented only once compared to re-exposed words. The coupling of spindles to slow oscillation peaks correlated with these differential effects on weaker and stronger memories. To gauge whether L-DOPA affects encoding or retrieval of information in addition to consolidation, we conducted a second experiment targeting L-DOPA only to initial encoding or retrieval and found no behavioural effects. Discussion: Our results demonstrate that L-DOPA augments slow wave sleep in elderly, perhaps tuning coordinated network activity and impacting the selection of information for long-term storage. The pharmaceutical modification of slowwave sleep and long-term memory may have clinical implications. [ABSTRACT FROM AUTHOR]

This document is a collection of late-breaking abstracts from the Journal of Sleep Research, covering a wide range of topics related to sleep disorders and their treatment. The abstracts discuss studies on the impact of sleep on cognitive abilities, memory problems in pregnant women, sleep markers after stroke, and the diagnosis of obstructive sleep apnea. Other studies explore the co-evolution of sleep oscillations and cognition, the prevalence of chronic insomnia, and the use of traditional Chinese medicine for anxiety symptoms. The document also includes studies on the use of technology in improving sleep quality, the effects of sleep disorders on various health conditions, and the use of co-production methodologies in sleep research. Additionally, there are studies on sleep problems in specific populations, such as commercial truck drivers and individuals with narcolepsy. The abstracts provide valuable insights into the understanding and treatment of sleep disorders, but further research is needed to validate and expand upon these findings. [Extracted from the article]

Summary Boosting slow‐wave activity (SWA) by modulating slow waves through closed‐loop auditory stimulation (CLAS) might provide a powerful non‐pharmacological tool to investigate the link between sleep and neurodegeneration. Here, we established mouse CLAS (mCLAS)‐mediated SWA enhancement and explored its effects on sleep deficits in neurodegeneration, by targeting the up‐phase of slow waves in mouse models of Alzheimer's disease (AD, Tg2576) and Parkinson's disease (PD, M83). We found that tracking a 2 Hz component of slow waves leads to highest precision of non‐rapid eye movement (NREM) sleep detection in mice, and that its combination with a 30° up‐phase target produces a significant 15–30% SWA increase from baseline in wild‐type (WTAD) and transgenic (TGAD) mice versus a mock stimulation group. Conversely, combining 2 Hz with a 40° phase target yields a significant increase ranging 30–35% in WTPD and TGPD mice. Interestingly, these phase‐target‐triggered SWA increases are not genotype dependent but strain specific. Sleep alterations that may contribute to disease progression and burden were described in AD and PD lines. Notably, pathological sleep traits were rescued by mCLAS, which elicited a 14% decrease of pathologically heightened NREM sleep fragmentation in TGAD mice, accompanied by a steep decrease in microarousal events during both light and dark periods. Overall, our results indicate that model‐tailored phase targeting is key to modulate SWA through mCLAS, prompting the acute alleviation of key neurodegeneration‐associated sleep phenotypes and potentiating sleep regulation and consolidation. Further experiments assessing the long‐term effect of mCLAS in neurodegeneration may majorly impact the establishment of sleep‐based therapies. [ABSTRACT FROM AUTHOR]

Objective: Sleep disturbance is common among individuals with eating disorders (EDs), with approximately 50% of patients with EDs reporting sleep disturbance. Sleep problems may promote, exacerbate, or maintain ED symptoms through a variety of hypothesized mechanisms, such as impaired executive function, increased negative affect, and disruptions to appetitive rhythms. Although research investigating the role of sleep in EDs is growing, the current literature suffers from methodological limitations and inconsistencies, which reduce our ability to translate findings to improve clinical practice. The purpose of this forum is to propose a coordinated approach to more seamlessly integrate sleep research into ED research with particular emphasis on best practices in the definition and assessment of sleep characteristics. Methods: In this article, we will describe the current status of sleep‐related research and relevant gaps within ED research practices, define key sleep characteristics, and review common assessment strategies for these sleep characteristics. Throughout the forum, we also discuss study design considerations and recommendations for future research aiming to integrate sleep research into ED research. Results/Discussion: Given the potential role of sleep in ED maintenance and treatment, it is important to build upon preliminary findings using a rigorous and systematic approach. Moving forward as a field necessitates a common lens through which future research on sleep and EDs may be conducted, communicated, and evaluated. [ABSTRACT FROM AUTHOR]

Depression and sleep disturbances are commonly seen non-motor symptoms in patients with Parkinson's disease (PD). This study used polysomnography to examine the relationship between mild-moderate depression in PD and sleep characteristics, particularly slow wave activities (SWA). 59 PD patients were split into two groups: nd-PD (n = 27) (patients with PD without depression) and d-PD (n = 32) (patients with PD with mild-moderate depression). Their clinical features, polysomnography parameters, and demographics were evaluated. Early and late sleep SWA spectrum densities and overnight SWA decline in different brain regions were particularly analyzed. Non-rapid eye movement 3 (N3) sleep duration and percentage were greater in the d-PD group. N3 percentage was linked to depression (p = 0.014). During late sleep, higher SWA (0.5–4Hz) in the frontal and central regions, higher low-SWA (0.5–2Hz) in the whole brain, central and occipital regions, and higher high-SWA (2–4Hz) in the frontal region was observed in the d-PD group. During early sleep, there was also higher low-SWA (0.5–2Hz) in the occipital region. Patients in d-PD group exhibited reduced overnight high-SWA (2–4Hz) decline (Δhigh-SWA) in the whole brain and occipital regions. Δhigh-SWA(2–4Hz) in the occipital region were associated with depression (p = 0.049). PD patients with mild-moderate depression have impaired slow wave sleep, exhibiting as increased N3 sleep, SWA, and reduced overnight SWA decline. This implies that synaptic strength reduction during sleep and impaired synaptic homeostasis regulation may be associated with depression in PD. Reduced overnight high-SWA decline in the occipital region may serve as a novel electrophysiological biomarker for indicating depression in PD. • PD patients with depression have impaired slow wave sleep and reduced overnight SWA decline. • Impaired synaptic homeostasis regulation may be associated with depression in PD. • Reduced overnight high-SWA decline may serve as a biomarker for indicating depression in PD. [ABSTRACT FROM AUTHOR]

Aims: To investigate changes in subjective and objective sleep quality after desmopressin administration in patients with nocturia due to nocturnal polyuria (NP) using electroencephalography (EEG) and the Pittsburgh sleep quality index (PSQI). Methods: Twenty male patients (≥65 years old) with NP participated in this study. The inclusion criteria were nocturnal frequency ≥ 2, NP index (NPi) ≥ 0.33, first uninterrupted sleep period (FUSP) ≤ 2.5 h, serum sodium concentration ≥ 135 mEq/L, and estimated glomerular filtration rate ≥ 50 mL/min/1.73 m2. Participants were given 50 μg of desmopressin to be taken orally once daily before bed. The primary endpoint was the change in the duration of slow‐wave sleep (nonrapid eye movement sleep stages 3 and 4), as evaluated by EEG 28 days from the baseline. The visual analog scale (VAS) was used as an additional indicator of sleep quality. Results: Analysis of data from 15 participants (median age: 74.0 [70.5, 76.0] years) revealed that from before to after desmopressin administration, significant decreases occurred in the median nocturnal frequency (3.0 [2.0, 4.0] to 1.5 [1.0, 2.0]) and NPi (0.445 [0.380, 0.475] to 0.360 [0.250, 0.430]). Furthermore, FUSP was significantly prolonged from 120.0 (94.0, 150.0) min to 210.0 (203.8, 311.3) min. Although the VAS scores improved, slow‐wave sleep duration and the PSQI global score showed no significant differences (68.50 [47.50, 75.50] and 48.00 [38.00, 66.50]; 5.0 [5.0, 10.0] and 7.0 [5.0, 9.0] min, respectively). Conclusion: Oral administration of 50 μg desmopressin improved nocturnal frequency and FUSP in older individuals with NP but did not significantly enhance sleep quality. In older adults, decreased nighttime urinary frequency may enhance quality of life; however, its influence on objective sleep quality may be limited. [ABSTRACT FROM AUTHOR]

Objectives. To compare the effects of fragmentation of stage 3 and REM sleep on melatonin (MT) secretion and to evaluate the effects of changes in the autonomic balance and activation reactions occurring in the slow-wave and REM sleep phases. Materials and Methods. Fifteen healthy men took part in three experiments: with fragmentation of stage 3, with fragmentation of REM sleep, and a control experiment in which sleep was not disturbed. In each experiment, seven saliva samples were collected in the evening, at night, and in the morning, and MT contents were determined. Heart rate variability was analyzed using electrocardiogram recordings and the autonomic balance was assessed. Results. Sleep fragmentation was accompanied by activation reactions and decreases in the durations of stage 3 sleep and REM sleep by 50% and 51% in the corresponding experiments. Fragmentation of REM sleep also led to an increase in the duration of nocturnal waking. Sleep disturbances caused an increase in MT secretion in the second half of the night and in the morning, which was particularly marked in the experiments with REM sleep fragmentation, in which MT on waking was 1.8 times higher than in the controls. Stage 3 fragmentation was accompanied by increased sympathetic activation, while REM sleep fragmentation did not cause autonomic shifts. Subjects were divided into two clusters: with high and low MT in night-time and morning saliva samples. In all experiments, subjects with high MT had nocturnal waking lasting 1.7–2 times longer, while these subjects had significantly more activations in the REM sleep phase in the experiments with fragmentation. Conclusions. Nocturnal sleep disturbances increased MT secretion, which was particularly marked with fragmentation of REM sleep. Increases in MT levels were not dependent on changes in the autonomic balance and appeared to be associated with activation of the serotoninergic system, which accompanies impairments of the depth and continuity of sleep. [ABSTRACT FROM AUTHOR]

Purpose: Coexisting dementia and rapid eye movement sleep behavior disorder (RBD) can negatively impact persons with dementia (PWD) and their family caregivers. Little research has investigated the relationship of sleep disturbance (i.e., RBD) in PWD–caregiver dyads who live together. Thus, we aimed to examine the impact of RBD symptoms on sleep quality of PWD and their family caregivers and describe sleep interrelationships. Method: This mixed methods study analyzed qualitative and quantitative data (wearable devices, semi-structured interviews, sleep diaries, and sleep quality surveys). Two dyads' sleep parameters and sleep experiences are reported. Results: Findings demonstrated that RBD symptoms in PWD affected sleep quality negatively (frequent awakening during the night and shortened deep sleep). Conclusion: Current findings highlight the importance of RBD assessment and management for PWD, as it could help improve caregivers' and PWDs' sleep quality and well-being. [Research in Gerontological Nursing, 17(5), 247–255.] [ABSTRACT FROM AUTHOR]

Sleep is a potential early, modifiable risk factor for cognitive decline and dementia. Impaired slow wave sleep (SWS) is pronounced in individuals with cognitive impairment (CI). Cognitive decline and impairments of SWS are bi-directionally linked in a vicious cycle. SWS can be enhanced non-invasively using phase-locked acoustic stimulation (PLAS), potentially breaking this vicious cycle. Eighteen healthy older adults (HC, agemean±sd, 68.3 ± 5.1) and 16 older adults (agemean±sd, 71.9 ± 3.9) with CI (Montreal Cognitive Assessment ≤ 25) underwent one baseline (sham-PLAS) night and three consecutive stimulation nights (real-PLAS). EEG responses and blood-plasma amyloid beta Aβ42/Aβ40 ratio were measured pre- and post-intervention, as was episodic memory. The latter was again evaluated 1 week and 3 months after the intervention. In both groups, PLAS induced a significant electrophysiological response in both voltage- and time–frequency analyses, and memory performance improved in association with the magnitude of this response. In the CI group, both electrophysiological and associated memory effects were delayed compared to the healthy group. After 3 intervention nights, electrophysiological response to PLAS was no longer different between CI and HC groups. Only in the CI sample, stronger electrophysiological responses were significantly associated with improving post-intervention Aβ42/Aβ40 ratios. PLAS seems to improve SWS electrophysiology, memory, and amyloid dynamics in older adults with CI. However, effects on memory require more time to unfold compared to healthy older adults. This indicates that PLAS may become a potential tool to ameliorate cognitive decline, but longer interventions are necessary to compensate for declining brain integrity. This study was pre-registered (clinicaltrials.gov: NCT04277104). [ABSTRACT FROM AUTHOR]

Objective To investigate the changes and features of firing activities of interneurons in dorsal hippocampus during the acquisition and consolidation of associative memory. Methods Trace eyeblink conditioning (tEBC) was utilized as a behavioral model of associative memory.A total of 18 wild-type C57BL/6 mice (male, 10~12 weeks old, weighing 22~25 g) were randomly divided into a paired group (n=9) and an unpaired group (n=9).Paired presentations of conditioned stimulus (CS) and unconditioned stimulus (US) were utilized to train these mice.The mice from the paired group were given US training in 250 ms after CS training, and those from the unpaired group received similar doses of CS and US training, but with no paired relationship in time.After 4 consecutive days'training, the mice of the paired group acquired tEBC, manifesting conditioned eyeblink responses (CR).Tetrode arrays were applied to record neuronal activity in dorsal hippocampus during both tEBC training epoch and the 1.5 h epoch after training.The putative interneurons (n=105) were identified according to their firing rate and spike width from trough to peak.Specific changes in hippocampal interneurons activity during tEBC training and post-training slow wave sleep were analyzed respectively. Results ① At the early stage of CR acquisition (the 1st and 2nd days), CS could evoke significantly greater activity of dorsal hippocampal interneurons in the paired group (P < 0.05).During sharp wave ripples (SWR) in the post-training slow wave sleep, the firing rate of dorsal hippocampal interneurons was significantly lower in the paired group than the unpaired group (P < 0.05).②At the late stage of CR acquisition (the 3rd and 4th days), no significant differences in CS evoked activity of dorsal hippocampal interneurons were observed between the paired group and unpaired group, neither in the firing rate of dorsal hippocampal interneurons during SWR in the post-training slow wave sleep between the 2 groups. Conclusion The dorsal hippocampal interneurons show opposite changes in firing activity during the acquisition and consolidation of associative memory.

According to the synaptic homeostasis hypothesis (SHY), sleep serves to renormalize synaptic connections that have been potentiated during the prior wake phase due to ongoing encoding of information. SHY focuses on glutamatergic synaptic strength and has been supported by numerous studies examining synaptic structure and function in neocortical and hippocampal networks. However, it is unknown whether synaptic down-regulation during sleep occurs in the hypothalamus, i.e., a pivotal center of homeostatic regulation of bodily functions including sleep itself. We show that sleep, in parallel with the synaptic down-regulation in neocortical networks, down-regulates the levels of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in the hypothalamus of rats. Most robust decreases after sleep were observed at both sites for AMPARs containing the GluA1 subunit. Comparing the effects of selective rapid eye movement (REM) sleep and total sleep deprivation, we moreover provide experimental evidence that slow-wave sleep (SWS) is the driving force of the down-regulation of AMPARs in hypothalamus and neocortex, with no additional contributions of REM sleep or the circadian rhythm. SWS-dependent synaptic down-regulation was not linked to EEG slow-wave activity. However, spindle density during SWS predicted relatively increased GluA1 subunit levels in hypothalamic synapses, which is consistent with the role of spindles in the consolidation of memory. Our findings identify SWS as the main driver of the renormalization of synaptic strength during sleep and suggest that SWS-dependent synaptic renormalization is also implicated in homeostatic control processes in the hypothalamus. Sleep normalizes synaptic connections in the cortex and hippocampus that have been potentiated during the preceding wake phase. This study shows that slow-wave sleep also down-regulates AMPA receptor levels in the hypothalamus, a brain region that regulates sleep. [ABSTRACT FROM AUTHOR]

One of the major breakthroughs of neurobiology was the identification of distinct ranges of oscillatory activity in the neuronal network that were found to be responsible for specific biological functions, both physiological and pathological in nature. Astrocytes, physically coupled by gap junctions and possessing the ability to simultaneously modulate the functions of a large number of surrounding synapses, are perfectly positioned to introduce synchronised oscillatory activity into the neural network. However, astrocytic somatic calcium signalling has not been investigated to date in the frequency ranges of common neuronal oscillations, since astrocytes are generally considered to be slow responders in terms of Ca2+ signalling. Using high-frequency two-photon imaging, we reveal fast Ca2+ oscillations in the soma of astrocytes in the delta (0.5–4 Hz) and theta (4–8 Hz) frequency bands in vivo in the rat cortex under ketamine–xylazine anaesthesia, which is known to induce permanent slow-wave sleep. The high-frequency astrocytic Ca2+ signals were not observed under fentanyl anaesthesia, excluding the possibility that the signals were introduced by motion artefacts. We also demonstrate that these fast astrocytic Ca2+ signals, previously considered to be exclusive to neurons, are present in a large number of astrocytes and are phase synchronised at the astrocytic network level. We foresee that the disclosure of these high-frequency astrocytic signals may help with understanding the appearance of synchronised oscillatory signals and may open up new avenues of treatment for neurological conditions characterised by altered neuronal oscillations. [ABSTRACT FROM AUTHOR]

Slow brain rhythms, for example during slow-wave sleep or pathological conditions like seizures and spreading depolarization, can be accompanied by oscillations in extracellular potassium concentration. Such slow brain rhythms typically have a lower frequency than tonic action-potential firing. They are assumed to arise from network-level mechanisms, involving synaptic interactions and delays, or from intrinsically bursting neurons. Neuronal burst generation is commonly attributed to ion channels with slow kinetics. Here, we explore an alternative mechanism generically available to all neurons with class I excitability. It is based on the interplay of fast-spiking voltage dynamics with a one-dimensional slow dynamics of the extracellular potassium concentration, mediated by the activity of the Na+/K+-ATPase. We use bifurcation analysis of the complete system as well as the slow-fast method to reveal that this coupling suffices to generate a hysteresis loop organized around a bistable region that emerges from a saddle-node loop bifurcation–a common feature of class I excitable neurons. Depending on the strength of the Na+/K+-ATPase, bursts are generated from pump-induced shearing the bifurcation structure, spiking is tonic, or cells are silenced via depolarization block. We suggest that transitions between these dynamics can result from disturbances in extracellular potassium regulation, such as glial malfunction or hypoxia affecting the Na+/K+-ATPase activity. The identified minimal mechanistic model outlining the sodium-potassium pump's generic contribution to burst dynamics can, therefore, contribute to a better mechanistic understanding of pathologies such as epilepsy syndromes and, potentially, inform therapeutic strategies. Author summary: The brain can produce slow rhythms, such as those observed during sleep or epilepsy. These rhythms are much slower than the neuronal electrical signals, and their origins are still under debate. Mechanisms discussed so far are often based on the connection delays in neural networks or on neuronal ion channels with particularly slow kinetics. We show that neurons with specific spiking dynamics–allowing them to fire at arbitrarily low frequencies (so-called class I neurons) can produce slow rhythmic patterns without requiring synaptic connectivity or special ion channels. In these cells, slow rhythmic activity arises from the interplay of slow changes in extracellular potassium concentration and the cell's voltage dynamics, mediated by the Na+/K+-ATPase pump. The latter, found in all neurons, regulates the concentrations of sodium and potassium ions across the cell membrane. The core mechanism is not idiosyncratic, rather mathematical analysis shows under which conditions slow rhythmic activity can arise generically from the pump-based coupling in a broad class of neurons. We demonstrate that the pump is relevant for the creation of different firing patterns, some of which have been associated with pathologies of the brain. A better mechanistic understanding of these complex, concentration-dependent dynamics can therefore be relevant for therapeutic approaches. [ABSTRACT FROM AUTHOR]

Sleep slow waves are the hallmark of deeper non-rapid eye movement sleep. It is generally assumed that gray matter properties predict slow-wave density, morphology, and spectral power in healthy adults. Here, we tested the association between gray matter volume (GMV) and slow-wave characteristics in 27 patients with moderate-to-severe traumatic brain injury (TBI, 32.0 ± 12.2 years old, eight women) and compared that with 32 healthy controls (29.2 ± 11.5 years old, nine women). Participants underwent overnight polysomnography and cerebral MRI with a 3 Tesla scanner. A whole-brain voxel–wise analysis was performed to compare GMV between groups. Slow-wave density, morphology, and spectral power (0.4–6 Hz) were computed, and GMV was extracted from the thalamus, cingulate, insula, precuneus, and orbitofrontal cortex to test the relationship between slow waves and gray matter in regions implicated in the generation and/or propagation of slow waves. Compared with controls, TBI patients had significantly lower frontal and temporal GMV and exhibited a subtle decrease in slow-wave frequency. Moreover, higher GMV in the orbitofrontal cortex, insula, cingulate cortex, and precuneus was associated with higher slow-wave frequency and slope, but only in healthy controls. Higher orbitofrontal GMV was also associated with higher slow-wave density in healthy participants. While we observed the expected associations between GMV and slow-wave characteristics in healthy controls, no such associations were observed in the TBI group despite lower GMV. This finding challenges the presumed role of GMV in slow-wave generation and morphology. [ABSTRACT FROM AUTHOR]

This article is a review on the effects of commonly used analgesics on sleep architecture. It discusses the bidirectional relationship between sleep and pain, as well as the negative effects of insufficient sleep on bodily functions. The authors focus on the effects of analgesics on sleep in patients with persistent pain and in healthy volunteers, including drugs such as paracetamol, NSAIDs, opioids, tricyclic and dual-action antidepressants, and gabapentinoids. The article provides a table summarizing the effects of these drugs on sleep parameters and pain levels. It emphasizes the importance of further research in this field to identify optimal treatment strategies. Additionally, there are two documents that provide references to scientific studies exploring the relationship between sleep and pain, as well as the effects of medications on sleep quality and pain. These studies offer valuable insights for researchers and individuals interested in understanding and managing these conditions. [Extracted from the article]

In mid-later life adults, early-onset and late-onset (i.e., onset ≥50 years) depression appear to be underpinned by different pathophysiology yet have not been examined in relation to autonomic function. Sleep provides an opportunity to examine the autonomic nervous system as the physiology changes across the night. Hence, we aimed to explore if autonomic profile is altered in mid-later life adults with remitted early-onset, late-onset and no history of lifetime depression. Participants aged 50–90 years (n = 188) from a specialised clinic underwent a comprehensive clinical assessment and completed an overnight polysomnography study. General Linear Models were used to examine the heart rate variability differences among the three groups for four distinct sleep stages and the wake after sleep onset. All analyses controlled for potential confounders – age, sex, current depressive symptoms and antidepressant usage. For the wake after sleep onset, mid-later life adults with remitted early-onset depression had reduced standard deviation of Normal to Normal intervals (SDNN; p =.014, d = −0.64) and Shannon Entropy (p =.004, d = −0.46,) than those with no history of lifetime depression. Further, the late-onset group showed a reduction in high-frequency heart rate variability (HF n.u.) during non-rapid eye movement sleep stage 2 (N2; p =.005, d = −0.53) and non-rapid eye movement sleep stage 3 (N3; p =.009, d = −0.55) when compared to those with no lifetime history. Causality between heart rate variability and depression cannot be derived in this cross-sectional study. Longitudinal studies are needed to examine the effects remitted depressive episodes on autonomic function. The findings suggest differential autonomic profile for remitted early-onset and late-onset mid-later life adults during sleep stages and wake periods. The differences could potentially serve as peripheral biomarkers in conjunction with more disease-specific markers of depression to improve diagnosis and prognosis. • Autonomic dysfunction is a key risk factor and symptom of major depressive disorder. • No known studies have examined the relationship between HRV and history of depression. • History of depression is associated with the integrity of autonomic functioning in mid-later life adults. • HRV has the potential to be a biomarker of depression. [ABSTRACT FROM AUTHOR]

Summary: The present study aimed to: (1) investigate sleep architecture in response to an overload training and taper periods among endurance runners; and (2) assess the sleep benefits of a high‐heat‐capacity mattress topper. Twenty‐one trained male endurance runners performed a 2‐week usual training regimen (baseline) followed by 2‐week overload and taper periods. From overload to the end of the taper period, they were assigned into two groups based on the mattress topper used: high‐heat‐capacity mattress topper (n = 11) or low‐heat‐capacity mattress topper (n = 10). Training load was assessed daily using the session rating of perceived exertion. Following each period, sleep was monitored by polysomnography, and nocturnal core body temperature was recorded throughout the night. Irrespective of the group, awakening episodes > 5 min decreased following overload compared with baseline (−0.48, p = 0.05). Independently of mattress topper, each 100 A.U. increase in 7‐day training load prior to polysomnographic recording was associated with higher slow‐wave sleep proportion (β = +0.13%; p = 0.05), lower sleep‐onset latency (β = −0.49 min; p = 0.05), and a reduction in the probability of transition from N1 sleep stage to wakefulness (β = −0.12%; p = 0.05). Sleeping on a high‐heat‐capacity mattress topper did not affect any sleep variable compared with a low‐heat‐capacity mattress topper. Increased training loads promote slow‐wave sleep and sleep propensity, highlighting the adaptative nature of sleep to diurnal activity and the role of sleep in physiological recovery. Further studies are required on the potential benefits of high‐heat‐capacity mattress toppers on sleep architecture among athletes. [ABSTRACT FROM AUTHOR]

Summary: Acute exercise has been shown to affect long‐term memory and sleep. However, it is unclear whether exercise‐induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep‐dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross‐over design. In two evening sessions, participants either exercised (high‐intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired‐associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High‐intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise‐induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise‐induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise‐induced sleep modifications and memory formation which requires further investigation in larger scaled studies. [ABSTRACT FROM AUTHOR]

Slow-wave sleep (SWS), characterized by slow oscillations (SOs, <1Hz) of alternating active and silent states in the thalamocortical network, is a primary brain state during Non-Rapid Eye Movement (NREM) sleep. In the last two decades, the traditional view of SWS as a global and uniform whole-brain state has been challenged by a growing body of evidence indicating that SO can be local and can coexist with wake-like activity. However, the mechanisms by which global and local SOs arise from micro-scale neuronal dynamics and network connectivity remain poorly understood. We developed a multi-scale, biophysically realistic human whole-brain thalamocortical network model capable of transitioning between the awake state and SWS, and we investigated the role of connectivity in the spatio-temporal dynamics of sleep SO. We found that the overall strength and a relative balance between long and short-range synaptic connections determined the network state. Importantly, for a range of synaptic strengths, the model demonstrated complex mixed SO states, where periods of synchronized global slow-wave activity were intermittent with the periods of asynchronous local slow-waves. An increase in the overall synaptic strength led to synchronized global SO, while a decrease in synaptic connectivity produced only local slow-waves that would not propagate beyond local areas. These results were compared to human data to validate probable models of biophysically realistic SO. The model producing mixed states provided the best match to the spatial coherence profile and the functional connectivity estimated from human subjects. These findings shed light on how the spatio-temporal properties of SO emerge from local and global cortical connectivity and provide a framework for further exploring the mechanisms and functions of SWS in health and disease. Author summary: Slow Wave Sleep (SWS) is a primary brain state found during Non-Rapid Eye Movement (NREM) sleep. While previously thought of as homogeneous waves of activity that sweep across the entire brain, recent research has suggested a more nuanced pattern of activity that can vary between local and global slow waves. However, understanding how these states emerge from small-scale neuronal dynamics and network connectivity remains unclear. We developed a biophysically realistic model of the human brain capable of generating SWS-like behavior and investigated the role of connectivity in the spatio-temporal dynamics of the sleep slow waves. We found that the overall strength and relative balance between long and short-range synaptic connections determined the network behavior—specifically, models with relatively weaker long-range connectivity resulted in mixed states of global and local slow waves. Comparing these results to human data, we found that models producing mixed states best matched the network behavior and functional connectivity observed in human subjects. These findings shed light on how the spatio-temporal properties of SWS emerge from local and global cortical connectivity and provide a framework for further exploring the mechanisms and functions of SWS in health and disease. [ABSTRACT FROM AUTHOR]

Research on slow-wave sleep (SWS) began almost a century ago, not long after the discovery of electroencephalography. From maintaining homeostasis to memory function, the pivotal role of SWS in health has been established. The elucidation of its mechanisms and functions is directly related to the fundamental question of why people sleep. This comprehensive review first summarizes the basic science of SWS from anatomical and physiological aspects. It describes the fundamental mechanisms and functions of SWS, including hormonal regulation, developmental changes in SWS across the lifespan, and associations between SWS and optimal physical, psychological, and cognitive functions. Next, the relationship between SWS and physical and mental disorders, for which increasing knowledge has accumulated in recent years, is discussed from both research and clinical perspectives. Conditions such as memory impairment, sleep-disordered breathing, neurodevelopmental disorders, and various psychiatric disorders are of concern. The relationship between SWS and the glymphatic system, which is responsible for waste clearance in the brain, has also been explored, highlighting the potential neuroprotective role of SWS. Finally, we discuss the future direction of the field regarding whether interventions in SWS can improve health. We also address the problem of the inconsistent definitions of SWS, slow-wave activity, and slow oscillations. This review emphasizes the importance of discussing SWS from both macro- and microarchitectural perspectives and highlights its potential clinical and research impacts. By reviewing these aspects, we aim to contribute to a deeper understanding of SWS and the future development of this research field. [ABSTRACT FROM AUTHOR]

The homeostatic regulation of sleep is characterized by rebound sleep after prolonged wakefulness, but the molecular and cellular mechanisms underlying this regulation are still unknown. In this study, we show that Ca2+/calmodulin-dependent protein kinase II (CaMKII)-dependent activity control of parvalbumin (PV)-expressing cortical neurons is involved in homeostatic regulation of sleep in male mice. Prolonged wakefulness enhances cortical PV-neuron activity. Chemogenetic suppression or activation of cortical PV neurons inhibits or induces rebound sleep, implying that rebound sleep is dependent on increased activity of cortical PV neurons. Furthermore, we discovered that CaMKII kinase activity boosts the activity of cortical PV neurons, and that kinase activity is important for homeostatic sleep rebound. Here, we propose that CaMKII-dependent PV-neuron activity represents negative feedback inhibition of cortical neural excitability, which serves as the distributive cortical circuits for sleep homeostatic regulation. The role of cortical PV neurons in the regulation of sleep architecture and homeostatic sleep rebound is not fully understood. Here, the authors show that CaMKII-mediated control of cortical parvalbumin-neuron activity regulates the homeostatic sleep rebound in mice. [ABSTRACT FROM AUTHOR]

Introduction: Reactivation of already consolidated memory can initiate its destabilization, making the memory trace labile. Normally, this destabilization is followed by reconsolidation of the memory trace, enriched by newly acquired experience. Disrupting the reconsolidation process, for example, by inhibiting protein synthesis, impairs subsequent memory retrieval, leading to reminderrelated amnesia. Previous studies in various species have shown that this impairment can be prevented by using NMDA receptor antagonists, which interfere with memory destabilization. Methods: In the present study we examined this phenomenon using a one-trial passive avoidance learning model in newborn chicks, the hypothesis being that inactivation of the NMDA-mediated transmission during memory reactivation would inhibit the memory trace labilization and thus prevent the reminderrelated amnesia. Results: We found that reminder-associated administration of the NMDA receptor antagonist MK-801 or one of the protein synthesis inhibitors (anisomycin, cycloheximide, 2-deoxygalactose) each alone produced amnesia. However, when combined, injection of MK-801 before the reminder prevented amnesia induced by protein synthesis inhibitors. Discussion: We suggest that the observed paradoxical effect implicates the involvement of NMDA receptors in both protein synthesis-independent engram destabilization upon its retrieval and protein synthesismediated engram stabilization after its updating. This puzzling dual role of NMDA receptors in memory destabilization/restabilization requires further investigation. [ABSTRACT FROM AUTHOR]

Sleep disorders are widespread. Inhaled aromatherapy has shown advantages over medication in treating insomnia. Daylily (Hemerocallis fulva) has been found to positively affect sleep either by ingestion or inhalation, but there is a lack of research on the sleep aid effect of its inhalation route. At present, the floral scent characteristics of daylily are not obvious, and the extraction rate of essential oil is low. Based on the above problems, this study developed daylily essence which replicates the natural aroma of plants and investigated the effect of inhaling daylily essence aroma on sleep activity by using Pittsburgh Sleep Quality Index (PSQI) and electroencephalogram (EEG). According to PSQI results, inhaling the aroma of daylily essence improved participants' subjective sleep quality. The difference between men and women was statistically significant (p <.05). The slow‐wave sleep activity of EEG in the experimental group was significantly stronger than that in the control group (p <.01). In addition, the frontal and central regions were more responsive to aroma stimuli (p <.05). The results of this study show that the aroma of daylily can promote the subjective and objective sleep quality of healthy college students, and the use of fragrance intervention is a potential scheme to improve sleep quality and insomnia. [ABSTRACT FROM AUTHOR]

Microglia sense the changes in their environment. How microglia actively translate these changes into suitable cues to adapt brain physiology is unknown. We reveal an activity-dependent regulation of cortical inhibitory synapses by microglia, driven by purinergic signaling acting on P2RX7 and mediated by microglia-derived TNFα.We demonstrate that sleep induces microgliadependent synaptic enrichment of GABAARs in a manner dependent on microglial TNFα and P2RX7. We further show that microglia-specific depletion of TNFα alters slow waves during NREM sleep and blunt memory consolidation in sleep-dependent learning tasks. Together, our results reveal that microglia orchestrate sleep-intrinsic plasticity of synaptic GABAARs, sculpt sleep slow waves, and support memory consolidation. [ABSTRACT FROM AUTHOR]

Objective: The authors report no conflicts of interest.To determine baseline sleep characteristics of male/female student-athletes across multiple sports using objective and subjective measures. Design: Prospective study. Setting: Division I college. Participants: Eighty-two male and female Division I student-athletes. Interventions: Participants completed 2 validated sleep questionnaires (Epworth Sleepiness Scale [ESS] and Single-Item Sleep Quality Scale [SISQS]) to assess subjective sleep. They also wore a validated sleep monitoring device (WHOOP 4.0 band) for at least 14 nights to collect objective data on total sleep time (TST) and sleep architecture. Main outcome measures: Overnight sleep variables, including TST, time spent awake in bed after falling asleep, time spent in light sleep, rapid eye movement (REM) sleep, and slow-wave sleep (SWS) cycles. Sleep quality and daytime sleepiness were also assessed. Results: There were no statistical differences between male and female student-athletes in average TST, sleep architecture, sleep consistency, SISQS, and ESS scores. The average TST was 409.2 ± 36.3 minutes. Sleep architecture consisted of 25.6% REM, 19.9% SWS, and 54.4% light sleep. The average sleep consistency was 61.6% ± 8.9%. The average SISQS score was 6.48 ± 1.71, and the average ESS score was 7.57 ± 3.82. A significant difference was found in average wake time between males and females (55.0 vs 43.7 min, P = 0.020), with an overall average of 50.2 ± 16.2 minutes. Conclusions: College student-athletes do not typically obtain the recommended amount of sleep. Optimizing sleep can positively affect academic and athletic performance. [ABSTRACT FROM AUTHOR]

Objective: Recent evidence shows that during slow‐wave sleep (SWS), the brain is cleared from potentially toxic metabolites, such as the amyloid‐beta protein. Poor sleep or elevated cortisol levels can worsen amyloid‐beta clearance, potentially leading to the formation of amyloid plaques, a neuropathological hallmark of Alzheimer disease. Here, we explored how nocturnal neural and endocrine activity affects amyloid‐beta fluctuations in the peripheral blood. Methods: We acquired simultaneous polysomnography and all‐night blood sampling in 60 healthy volunteers aged 20–68 years. Nocturnal plasma concentrations of amyloid‐beta‐40, amyloid‐beta‐42, cortisol, and growth hormone were assessed every 20 minutes. Amyloid‐beta fluctuations were modeled with sleep stages, (non)oscillatory power, and hormones as predictors while controlling for age and participant‐specific random effects. Results: Amyloid‐beta‐40 and amyloid‐beta‐42 levels correlated positively with growth hormone concentrations, SWS proportion, and slow‐wave (0.3–4Hz) oscillatory and high‐band (30–48Hz) nonoscillatory power, but negatively with cortisol concentrations and rapid eye movement sleep (REM) proportion measured 40–100 minutes previously (all t values > |3|, p values < 0.003). Older participants showed higher amyloid‐beta‐40 levels. Interpretation: Slow‐wave oscillations are associated with higher plasma amyloid‐beta levels, whereas REM sleep is related to decreased amyloid‐beta plasma levels, possibly representing changes in central amyloid‐beta production or clearance. Strong associations between cortisol, growth hormone, and amyloid‐beta presumably reflect the sleep‐regulating role of the corresponding releasing hormones. A positive association between age and amyloid‐beta‐40 may indicate that peripheral clearance becomes less efficient with age. ANN NEUROL 2024;96:46–60 [ABSTRACT FROM AUTHOR]

The aim was to investigate brain responses to non-painful tactile stimuli applied to the non-dominant hand during sleep. 21 healthy subjects participated in the study (11 female, mean age ± SD: 20.67 ± 1.91 years). A 40-channel polysomnography system and a pneumatic tactile stimulator unit were used. Stimuli were applied to the participants' non-dominant hand. Evoked potential components of the CZ electrode were examined in four sleep stages (N1, N2, N3, and REM). Repeated measures ANOVA was used in statistical analyses. Brain responses, categorized as early (P50, N100, and P200), mid-early (N300, P450, and N550), and late (P900 and Nlate), were detected all sleep stages. No notable variances were found in the amplitude and latency of early brain responses when analyzed across different sleep stages. Differences in both amplitude and latency were observed across different sleep stages for the N300, P450, P900, and Nlate response components. This study presents a pioneering exploration into the responses of the non-dominant hand throughout all sleep stages, encompassing eight distinct response components. This novel investigation contributes to the existing literature by shedding light on previously unexplored aspects. The observed early responses are identified as sensory, while middle to late responses align with cognitive processes within the realm of sleep research. Notably, N300, P450, P900, and Nlate components display variations across diverse sleep stages, marked by alterations in both amplitude and latency. These findings offer valuable insights into the dynamic nature of hand responses throughout the sleep continuum. [ABSTRACT FROM AUTHOR]

Sleep stages can provide valuable insights into an individual's sleep quality. By leveraging movement and heart rate data collected by modern smartwatches, it is possible to enable the sleep staging feature and enhance users' understanding about their sleep and health conditions. In this paper, we present and validate a recurrent neural network based model with 23 input features extracted from accelerometer and photoplethysmography sensors data for both healthy and sleep apnea populations. We designed a lightweight and fast solution to enable the prediction of sleep stages for each 30-s epoch. This solution was developed using a large dataset of 1522 night recordings collected from a highly heterogeneous population and different versions of Samsung smartwatch. In the classification of four sleep stages (wake, light, deep, and rapid eye movements sleep), the proposed solution achieved 71.6 % of balanced accuracy and a Cohen's kappa of 0.56 in a test set with 586 recordings. The results presented in this paper validate our proposal as a competitive wearable solution for sleep staging. Additionally, the use of a large and diverse data set contributes to the robustness of our solution, and corroborates the validation of algorithm's performance. Some additional analysis performed for healthy and sleep apnea population demonstrated that algorithm's performance has low correlation with demographic variables. • Proposal and evaluation of a smartwatch-based solution for sleep staging. • Experimental evaluation on a large and diverse dataset of 1522 sleep recordings. • Solution based on neural networks trained on accelerometer and PPG sensor data. • 71.6 % of balanced accuracy for classification of 4 sleep stages compared with PSG. • Low correlation of performance with demographic variables and sleep apnea disorder. [ABSTRACT FROM AUTHOR]