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"Sleep-wake cycle"
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Baby animals day & night
Introduces diurnal and nocturnal animals in pretty black and white images, perfect for developing eyes.
Book
Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruning
Aging is associated with loss of circadian immune responses and circadian gene transcription in peripheral macrophages. Microglia, the resident macrophages of the brain, also show diurnal rhythmicity in regulating local immune responses and synaptic remodeling. To investigate the interaction between aging and microglial circadian rhythmicity, we examined mice deficient in the core clock transcription factor, BMAL1. Aging
Cd11b
cre
;Bmal
lox/lox
mice demonstrated accelerated cognitive decline in association with suppressed hippocampal long-term potentiation and increases in immature dendritic spines. C1q deposition at synapses and synaptic engulfment were significantly decreased in aging
Bmal1
-deficient microglia, suggesting that BMAL1 plays a role in regulating synaptic pruning in aging. In addition to accelerated age-associated hippocampal deficits,
Cd11b
cre
;Bmal
lox/lox
mice also showed deficits in the sleep–wake cycle with increased wakefulness across light and dark phases. These results highlight an essential role of microglial BMAL1 in maintenance of synapse homeostasis in the aging brain.
Journal Article
Nonlinear relationship between sleep midpoint and depression symptoms: a cross-sectional study of US adults
Background
Despite the close relationship between sleep–wake cycles and depression symptoms, the relationship between sleep midpoint and depression symptoms in adults remains understudied.
Methods
In this cross-sectional study, 18280 adults aged ≥ 18 years from the National Health and Nutrition Examination Survey (NHANES) 2015–2020 were analyzed. Covariates included age, sex, race/ethnicity, education level, marital status, family income, body mass index, smoking status, drinking status, physical activity, comorbid condition, sleep duration, and sleep disturbance were adjusted in multivariate regression models.
Results
Weighted restricted cubic spline based on the complex sampling design of NHANES showed that in participants with a sleep midpoint from 2:18 AM to 6:30 AM, the prevalence of depression symptoms increased by 0.2 times (adjusted odds ratio [OR] = 1.20, 95% confidence interval [CI]: 1.08–1.33) per 1-h increment in sleep midpoint compared to the reference point of 2:18 AM. For participants with a sleep midpoint after 6:30 AM and before 2:18 AM the next day, the relationship between sleep midpoint and depression symptoms was not significant after adjusting for all covariates (adjusted OR = 1.01, 95% CI: 0.99–1.03).
Conclusions
The findings indicate a significant nonlinear association between sleep midpoint and depression symptoms in a nationally representative sample of adults.
Journal Article
Haplotype of the astrocytic water channel AQP4 is associated with slow wave energy regulation in human NREM sleep
Cerebrospinal fluid (CSF) flow through the brain parenchyma is facilitated by the astrocytic water channel aquaporin 4 (AQP4). Homeostatically regulated electroencephalographic (EEG) slow waves are a hallmark of deep non-rapid eye movement (NREM) sleep and have been implicated in the regulation of parenchymal CSF flow and brain clearance. The human AQP4 gene harbors several single nucleotide polymorphisms (SNPs) associated with AQP4 expression, brain-water homeostasis, and neurodegenerative diseases. To date, their role in sleep-wake regulation is unknown. To investigate whether functional variants in AQP4 modulate human sleep, nocturnal EEG recordings and cognitive performance were investigated in 123 healthy participants genotyped for a common eight-SNP AQP4-haplotype. We show that this AQP4-haplotype is associated with distinct modulations of NREM slow wave energy, strongest in early sleep and mirrored by changes in sleepiness and reaction times during extended wakefulness. The study provides the first human evidence for a link between AQP4, deep NREM sleep, and cognitive consequences of prolonged wakefulness.
Journal Article
Crosstalk between metabolism and circadian clocks
Humans, like all mammals, partition their daily behaviour into activity (wakefulness) and rest (sleep) phases that differ largely in their metabolic requirements. The circadian clock evolved as an autonomous timekeeping system that aligns behavioural patterns with the solar day and supports the body functions by anticipating and coordinating the required metabolic programmes. The key component of this synchronization is a master clock in the brain, which responds to light–darkness cues from the environment. However, to achieve circadian control of the entire organism, each cell of the body is equipped with its own circadian oscillator that is controlled by the master clock and confers rhythmicity to individual cells and organs through the control of rate-limiting steps of metabolic programmes. Importantly, metabolic regulation is not a mere output function of the circadian system, but nutrient, energy and redox levels signal back to cellular clocks in order to reinforce circadian rhythmicity and to adapt physiology to temporal tissue-specific needs. Thus, multiple systemic and molecular mechanisms exist that connect the circadian clock with metabolism at all levels, from cellular organelles to the whole organism, and deregulation of this circadian–metabolic crosstalk can lead to various pathologies.Circadian rhythms align organismal functions with phases of rest and activity. Accordingly, circadian oscillations occur in many physiological processes, including various metabolic functions. In turn, metabolic cues are emerging as regulators of the circadian clock. This crosstalk between metabolism and circadian rhythms has important implications for human health.
Journal Article
Interplay between circadian rhythm, ageing and neurodegenerative disorder
Circadian rhythm, as a homeostatic tool of biological life, plays a vital role in regulating human physiology, metabolism, endocrinology, and emotional and cognitive behaviour. A disrupted circadian rhythm, marked by age-related alterations such as decreased variation in sleep–wake patterns and instability in the timing of these patterns, can worsen age-related problems such as increased oxidative stress and inflammation. Advancing age is associated with anomalies in the redox balance, gradual alterations in physiological functions and deregulation of various metabolic pathways. The mutual interaction between circadian rhythm and ageing may potentially contribute to the development of neurodegenerative disorders. Consistent alterations in circadian rhythms could lead to various degenerative disorders and aggravate age-related ailments. Therefore, understanding and unravelling the intricate interplay between circadian rhythm and ageing holds immense potential for developing therapeutic interventions and promoting healthy ageing strategies. In this review article, we discuss the role of circadian rhythms in physiology and their age-related changes that impact health. We focus on how disruptions in circadian rhythms, common with ageing, may increase risks for neurodegenerative disorders. Understanding this interaction holds promise for developing therapeutic approaches to support healthy ageing.
Journal Article
Blue-enriched office light competes with natural light as a zeitgeber
Objectives Circadian regulation of human physiology and behavior (eg, body temperature or sleep-timing), depends on the \"zeitgeber\" light that synchronizes them to the 24-hour day. This study investigated the effect of changing light temperature at the workplace from 4000 Kelvin (K) to 8000 K on sleep—wake and activity—rest behavior. Methods An experimental group (N=27) that experienced the light change was compared with a non-intervention group (N=27) that remained in the 4000 K environment throughout the 5-week study period (14 January to 17 February). Sleep logs and actimetry continuously assessed sleep—wake behavior and activity patterns. Results Over the study period, the timing of sleep and activity on free days steadily advanced parallel to the seasonal progression of sunrise in the non-intervention group. In contrast, the temporal pattern of sleep and activity in the experimental group remained associated with the constant onset of work. Conclusion The results suggest that artificial blue-enriched light competes with natural light as a zeitgeber. While subjects working under the warmer light (4000 K) appear to entrain (or synchronize) to natural dawn, the subjects who were exposed to blue-enriched (8000 K) light appear to entrain to office hours. The results confirm that light is the dominant zeitgeber for the human clock and that its efficacy depends on spectral composition. The results also indicate that blue-enriched artificial light is a potent zeitgeber that has to be used with diligence.
Journal Article
Effects of the dual orexin receptor antagonist DORA-22 on sleep in 5XFAD mice
Sleep disruption is a characteristic of Alzheimer's disease (AD) that may exacerbate disease progression. This study tested whether a dual orexin receptor antagonist (DORA) would enhance sleep and attenuate neuropathology, neuroinflammation, and cognitive deficits in an AD-relevant mouse model, 5XFAD.
Wild-type (C57Bl6/SJL) and 5XFAD mice received chronic treatment with vehicle or DORA-22. Piezoelectric recordings monitored sleep and spatial memory was assessed via spontaneous Y-maze alternations. Aβ plaques, Aβ levels, and neuroinflammatory markers were measured by immunohistochemistry, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction, respectively.
In 5XFAD mice, DORA-22 significantly increased light-phase sleep without reducing Aβ levels, plaque density, or neuroinflammation. Effects of DORA-22 on cognitive deficits could not be determined because the 5XFAD mice did not exhibit deficits.
These findings suggest that DORAs may improve sleep in AD patients. Further investigations should optimize the dose and duration of DORA-22 treatment and explore additional AD-relevant animal models and cognitive tests.
•Daily DORA-22 treatment at light onset for 5 weeks increased sleep in 5XFAD mice.•DORA-22 mainly increased sleep during the light (inactive) phase.•Chronic DORA-22 treatment did not affect cortical amyloid β levels or plaques.•Chronic DORA-22 treatment did not alter cortical neuroinflammation.
Journal Article
Adenosine: A Mediator of the Sleep-Inducing Effects of Prolonged Wakefulness
Both subjective and electroencephalographic arousal diminish as a function of the duration of prior wakefulness. Data reported here suggest that the major criteria for a neural sleep factor mediating the somnogenic effects of prolonged wakefulness are satisfied by adenosine, a neuromodulator whose extracellular concentration increases with brain metabolism and which, in vitro, inhibits basal forebrain cholinergic neurons. In vivo microdialysis measurements in freely behaving cats showed that adenosine extracellular concentrations in the basal forebrain cholinergic region increased during spontaneous wakefulness as contrasted with slow wave sleep; exhibited progressive increases during sustained, prolonged wakefulness; and declined slowly during recovery sleep. Furthermore, the sleep-wakefulness profile occurring after prolonged wakefulness was mimicked by increased extracellular adenosine induced by microdialysis perfusion of an adenosine transport inhibitor in the cholinergic basal forebrain but not by perfusion in a control noncholinergic region.
Journal Article
Promoting arousal associated with physical activity with the vitamin B1 derivative TTFD
Physical inactivity, which is a global issue, reduces physical and mental vitality, particularly impairing prefrontal-cortex-based mental health. This may trigger social withdrawal and depression, hindering the ability to have an active lifestyle. However, we have identified a beneficial agent, a vitamin B1 derivative called thiamine tetrahydrofurfuryl disulfide (TTFD), that enhances physical activity through dopaminergic regulation in the medial prefrontal cortex (mPFC) of rats. Since the brain dopaminergic system also regulates the sleep-wake cycle via the ascending arousal system, we postulated that TTFD may promote arousal. To test this, we performed electroencephalograms and electromyograms in rats, monitoring their physical activity and sleep-wake cycles after TTFD injection. Analysis revealed that TTFD acutely promotes arousal, reduces slow-wave sleep (SWS) and rapid eye movement (REM) sleep, and promotes increased physical activity. TTFD not only promotes physical activity but also increases arousal, thereby potentially contributing to enhanced mental health.
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Journal Article