Epilepsy and Its Interaction With Sleep and Circadian Rhythm.
Ontology highlight
ABSTRACT:
SUBMITTER: Jin B
PROVIDER: S-EPMC7225332 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
Publications
Epilepsy and Its Interaction With Sleep and Circadian Rhythm.
Jin Bo B Aung Thandar T Geng Yu Y Wang Shuang S
Frontiers in neurology 20200508
Growing evidence shows the bidirectional interactions between sleep, circadian rhythm, and epilepsy. Comprehending how these interact with each other may help to advance our understanding of the pathophysiology of epilepsy and develop new treatment strategies to improve seizure control by reducing the medication side effects and the risks associated with seizures. In this review, we present the overview of different temporal patterns of interictal epileptiform discharges and epileptic seizures o ...[more]
Similar Datasets
Project description:MicroRNAs are important coordinators of circadian regulation that mediate the fine-tuning of gene expression. Although many studies have shown the effects of individual miRNAs on the circadian clock, the global functional miRNA-mRNA interaction network involved in the circadian system remains poorly understood. Here, we used CLEAR (Covalent Ligation of Endogenous Argonaute-bound RNAs)-CLIP (Cross-Linking and Immuno-Precipitation) to explore the regulatory functions of miRNAs in the circadian system by comparing the miRNA-mRNA interactions between Drosophila wild-type strain W1118 and a mutant of the key circadian transcriptional regulator Clock (Clkjrk ). This experimental approach unambiguously identified tens of thousands of miRNA-mRNA interactions in both the head and body. The miRNA-mRNA interactome showed dramatic changes in the Clkjrk flies. Particularly, among ~300 miRNA-mRNA circadian relevant interactions, multiple interactions involving core clock genes pdp1, tim, and vri displayed distinct changes as a result of the Clk mutation. Based on the CLEAR-CLIP analysis, we found a novel regulation of the circadian rhythm and sleep by the miR-375-timeless interaction. The results indicated that Clk disruption abolished normal rhythmic expression of miR-375 and the functional regulation occurred in the l-LNv neurons, where miR-375 modulated the circadian rhythm and sleep via targeting timeless. This work provides the first global view of miRNA regulation in the circadian rhythm.
| S-EPMC8805441 | biostudies-literature
Project description:Sleep disturbances are recognized as a common nonmotor complaint in Parkinson disease but their etiology is poorly understood.To define the sleep and circadian phenotype of patients with early-stage Parkinson disease.Initial assessment of sleep characteristics in a large population-representative incident Parkinson disease cohort (N=239) at the University of Cambridge, England, followed by further comprehensive case-control sleep assessments in a subgroup of these patients (n=30) and matched controls (n=15).Sleep diagnoses and sleep architecture based on polysomnography studies, actigraphy assessment, and 24-hour analyses of serum cortisol, melatonin, and peripheral clock gene expression (Bmal1, Per2, and Rev-Erb?).Subjective sleep complaints were present in almost half of newly diagnosed patients and correlated significantly with poorer quality of life. Patients with Parkinson disease exhibited increased sleep latency (P?=?.04), reduced sleep efficiency (P?=?.008), and reduced rapid eye movement sleep (P?=?.02). In addition, there was a sustained elevation of serum cortisol levels, reduced circulating melatonin levels, and altered Bmal1 expression in patients with Parkinson disease compared with controls.Sleep dysfunction seen in early Parkinson disease may reflect a more fundamental pathology in the molecular clock underlying circadian rhythms.
| S-EPMC4119609 | biostudies-literature
Project description:We evaluated the circadian phenotypes of patients with delayed sleep-wake phase disorder (DSWPD) and non-24-hour sleep-wake rhythm disorder (N24SWD), two different circadian rhythm sleep disorders (CRSDs) by measuring clock gene expression rhythms in fibroblast cells derived from individual patients. Bmal1-luciferase (Bmal1-luc) expression rhythms were measured in the primary fibroblast cells derived from skin biopsy samples of patients with DSWPD and N24SWD, as well as control subjects. The period length of the Bmal1-luc rhythm (in vitro period) was distributed normally and was 22.80±0.47 (mean±s.d.) h in control-derived fibroblasts. The in vitro periods in DSWPD-derived fibroblasts and N24SWD-derived fibroblasts were 22.67±0.67 h and 23.18±0.70 h, respectively. The N24SWD group showed a significantly longer in vitro period than did the control or DSWPD group. Furthermore, in vitro period was associated with response to chronotherapy in the N24SWD group. Longer in vitro periods were observed in the non-responders (mean±s.d.: 23.59±0.89 h) compared with the responders (mean±s.d.: 22.97±0.47 h) in the N24SWD group. Our results indicate that prolonged circadian periods contribute to the onset and poor treatment outcome of N24SWD. In vitro rhythm assays could be useful for predicting circadian phenotypes and clinical prognosis in patients with CRSDs.
| S-EPMC5416712 | biostudies-literature
Project description:Circadian (?24-hour) timing systems pervade all kingdoms of life and temporally optimize behavior and physiology in humans. Relatively recent changes to our environments, such as the introduction of artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behavior and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these, too, are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioral and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important.
| S-EPMC5142605 | biostudies-literature
Project description:BackgroundIndividuals with typical circadian rhythm sleep-wake disorders (CRSWDs) have a habitual sleep timing that is desynchronized from social time schedules. However, it is possible to willfully force synchronisation against circadian-driven sleepiness, which causes other sleep problems. This pathology is distinguishable from typical CRSWDs and is referred to here as latent CRSWD (LCRSWD). Conventional diagnostic methods for typical CRSWDs are insufficient for detecting LCRSWD because sufferers have an apparently normal habitual sleep timing.MethodsWe first evaluated the reliability of circadian phase estimation based on clock gene expression using hair follicles collected at three time points without sleep interruption. Next, to identify detection criteria for LCRSWD, we compared circadian and sleep parameters according to estimated circadian phases, at the group and individual level, between subjects with low and high Pittsburgh Sleep Quality Index (PSQI) scores. To validate the reliability of identified detection criteria, we investigated whether the same subjects could be reproducibly identified at a later date and whether circadian amelioration resulted in sleep improvement.FindingsWe successfully validated the reliability of circadian phase estimation at three time points and identified potential detection criteria for individuals with LCRSWD attributed to delayed circadian-driven sleepiness. In particular, a criterion based on the interval between the times of the estimated circadian phase of clock gene expression and getting out of bed on work or school days was promising. We also successfully confirmed the reproducibility of candidate screening and sleep improvement by circadian amelioration, supporting the reliability of the detection criteria.InterpretationAlthough several limitations remain, our present study demonstrates a promising prototype of a detection method for LCRSWD attributed to delayed circadian-driven sleepiness. More extensive trials are needed to further validate this method.FundingThis study was supported mainly by JSPS, Japan.
| S-EPMC7653065 | biostudies-literature
Project description:IntroductionSleep and rest-activity rhythm alterations are common in neurodegenerative diseases. However, their characterization in patients with behavioral variant frontotemporal dementia (bvFTD) has proven elusive. We investigated rest-activity rhythm alterations, sleep disturbances, and their neural correlates in bvFTD.MethodsTwenty-seven bvFTD patients and 25 healthy controls completed sleep questionnaires and underwent 7 days of actigraphy while concurrently maintaining a sleep diary. Cortical complexity and thickness were calculated from T1-weighted magnetic resonance (MR) images.ResultsCompared to controls, bvFTD patients showed longer time in bed (95% confidence interval [CI]: 79.31, 321.83) and total sleep time (95% CI: 24.38, 321.88), lower sleep efficiency (95% CI: -12.58, -95.54), and rest-activity rhythm alterations in the morning and early afternoon. Increased sleep duration was associated with reduced cortical thickness in frontal regions.DiscussionPatients with bvFTD showed longer sleep duration, lower sleep quality, and rest-activity rhythm alterations. Actigraphy could serve as a cost-effective and accessible tool for ecologically monitoring changes in sleep duration in bvFTD patients.HighlightsWe assessed sleep and circadian rhythms in behavioral variant frontotemporal dementia (bvFTD) using actigraphy. Patients with bvFTD show increased sleep duration and reduced sleep quality. Patients with bvFTD show rest-activity alterations in the morning and early afternoon. Sleep duration is associated with reduced cortical thickness in frontal regions. These alterations may represent an early sign of neurodegeneration.
| S-EPMC10984421 | biostudies-literature
Project description:Shift workers and many other groups experience irregular sleep-wake patterns. This can induce excessive daytime sleepiness that decreases productivity and elevates the risk of accidents. However, the degree of daytime sleepiness is not correlated with standard sleep parameters like total sleep time, suggesting other factors are involved. Here, we analyze real-world sleep-wake patterns of shift workers measured with wearables by developing a computational package that simulates homeostatic sleep pressure - physiological need for sleep - and the circadian rhythm. This reveals that shift workers who align sleep-wake patterns with their circadian rhythm have lower daytime sleepiness, even if they sleep less. The alignment, quantified by the sleep parameter, circadian sleep sufficiency, can be increased by dynamically adjusting daily sleep durations according to varying bedtimes. Our computational package provides flexible and personalized real-time sleep-wake patterns for individuals to reduce their daytime sleepiness and could be used with wearables to develop smart alarms.
| S-EPMC8479255 | biostudies-literature
Project description:Alzheimer's disease (AD) was discovered and the pathological hallmarks were revealed more than a century ago. Subsequently, many remarkable discoveries and breakthroughs provided us with mechanistic insights into the pathogenesis of AD. The identification of the molecular underpinning of the disease not only provided the framework of AD pathogenesis but also targets for therapeutic inventions. Despite all the initial successes, no effective treatment for AD has emerged yet as all the late stages of clinical trials have failed. Many factors ranging from genetic to environmental factors have been critically appraised as the potential causes of AD. In particular, the role of stress on AD has been intensively studied while the relationship between sleep and circadian rhythm disruption (SCRD) and AD have recently emerged. SCRD has always been thought to be a corollary of AD pathologies until recently, multiple lines of evidence converge on the notion that SCRD might be a contributing factor in AD pathogenesis. More importantly, how stress and SCRD intersect and make their concerted contributions to AD phenotypes has not been reviewed. The goal of this literature review is to examine at multiple levels - molecular, cellular (e.g. microglia, gut microbiota) and holistic - how the interaction between stress and SCRD bi-directionally and synergistically exacerbate AD pathologies and cognitive impairment. AD, in turn, worsens stress and SCRD and forms the vicious cycle that perpetuates and amplifies AD.
| S-EPMC6279965 | biostudies-literature
Project description:ObjectiveOrganic light-emitting diodes (OLEDs) emit less blue light than traditional light-emitting diodes (LEDs), and we previously found that early-night OLED light exposure (LE) delays the melatonin phase by less than LED at a color temperature of 4,000 K. As a follow-up study, we investigated the effects of OLED and LED at a different color temperature (3,000 K) on melatonin profile, sleep, and vigilance.Methods24 healthy subjects (27.5±5.1 years) were exposed to three light conditions [OLED, LED, and dim light (DL)] from 17:30 to 24:00, in a random order and with a 1-week interval. Saliva samples for melatonin were taken every hour from 18:00 to 24:00. Polysomnography (PSG) and a psychomotor vigilance test (PVT) were performed.ResultsMelatonin onset time was significantly delayed under OLED and LED compared with DL, with no significant difference between OLED and LED. The mean melatonin level at 24:00 under LED was lower than that under DL, but there was no significant difference between OLED LE and DL. The percentage of slow wave sleep (N3) in LED was significantly lower than in OLED.ConclusionExposure to light in the evening can suppress melatonin secretion late at night and disturb deep sleep, and those effects are slightly worse under LED than OLED.
| S-EPMC8169338 | biostudies-literature
Project description:The circadian rhythm, called Process C, regulates a wide range of biological processes in humans including sleep, metabolism, body temperature, and hormone secretion. Light is the dominant synchronizer of the circadian rhythm-it has been used to regulate the circadian phase to cope with jet-lag, shift work, and sleep disorder. The homeostatic oscillation of the sleep drive is called Process S. Process C and Process S together determine the sleep-wake cycle in what is known as the two-process model. This paper addresses the regulation of both Process C and Process S by scheduling light exposure and sleep based on numerical simulations of circadian rhythm and sleep mathematical models. This is a significant step beyond the existing literature that only considers the entrainment of Process C. Regulation of the two-process model poses several unique features and challenges: 1. Process S is non-smooth, i.e., the homeostatic dynamics are different in the sleep and wake regimes; 2. Light only indirectly affects Process S through Process C; 3. Light does not affect Process C during sleep. We consider two scenarios: optimizing light intensity as the control input with spontaneous (i.e., unscheduled) sleep/wake times and jointly optimizing the light intensity and the sleep/wake times, which allows limited delayed sleep and early waking as part of the decision variables. We solve the time-optimal entrainment problem for the two-process model for both scenarios using an extension of the gradient descent algorithm to non-smooth systems. To illustrate the efficacy of our time-optimal entrainment strategies, we consider two common use cases: transmeridian travelers and shift workers. For transmeridian travelers, joint optimization of the two-process model avoids the unrealistic long wake duration when only Process C is considered. The entrainment time also decreases when both the light input and the sleep schedule are optimized compared to when only the light input is optimized. For shift workers, we show that the entrainment time is significantly shortened by optimizing the night shift working light.
| S-EPMC8186815 | biostudies-literature