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This commentary highlights the critical role of sleep as a public health issue, particularly during a stressful life period such as the COVID-19 pandemic, and provides evidence-based practical guidelines to manage sleep disturbances during this crisis. The COVID-19 pandemic and the imposed social confinement have produced significant stress, anxiety, and worries about health and the fear of being infected, jobs and financial problems, and uncertainty about the future. The incidence of sleep disturbances has also increased dramatically during this period. Aside from stress and anxiety, two other factors are likely to contribute to increased sleep disturbances during this crisis. First, alterations of our daily routines such as arising at a specific time, showing up at work, eating, exercising, and engaging in social and leisure activities at relatively fixed times are all important timekeepers for our sleep-wake cycles to remain synchronized with the day (light) and night (dark) cycles. Alterations of these timekeepers, combined with reduced daylight exposure, also essential to keep our biological clock synchronized, are likely to disrupt sleep and circadian rhythms. Sleep plays a fundamental role for mental and physical health, and adequate sleep duration and quality are essential for coping with major life events such as the COVID-19 pandemic. Public health education is warranted to keep the population well informed about the importance of sleep and healthy sleep practices in order to cope with the pandemic and prevent or minimize long-term adverse outcomes.

[...]studies consistently show that sleep continuity, slow-wave sleep (SWS), REM sleep, K-complexes, and sleep spindles have specific and essential roles in neurogenesis (14), synaptic plasticity (15), and next-day vigilance (16), as well as in memory formation and consolidation (17, 18). [...]apneas and hypopneas provoke adaptive (e.g., ischemic preconditioning) but also maladaptive and potentially harmful responses (e.g., oxidative stress, inflammation, hypertension, dysautonomia, impaired glucose tolerance, and blood-brain barrier dysfunction) that may damage cerebral cells and organelles, and make neurons more susceptible to cellular death (32). [...]OSA might be a risk factor for cognitive decline in neurodegenerative disorders, with the predominant pathology and clinical manifestations depending on predisposing factors. [...]exercise training has been described as having positive effects on OSA severity in sedentary overweight/obese young and middleaged adults (70). [...]we need to verify whether physical activity can reduce Aß deposition, as previously described in nonapneic participants (71). * Another line of research is to clarify the mechanistic processes that link OSA to dementia, to identify novel targets for intervention.

Sleep benefits motor memory consolidation. This mnemonic process is thought to be mediated by thalamo-cortical spindle activity during NREM-stage2 sleep episodes as well as changes in striatal and hippocampal activity. However, direct experimental evidence supporting the contribution of such sleep-dependent physiological mechanisms to motor memory consolidation in humans is lacking. In the present study, we combined EEG and fMRI sleep recordings following practice of a motor sequence learning (MSL) task to determine whether spindle oscillations support sleep-dependent motor memory consolidation by transiently synchronizing and coordinating specialized cortical and subcortical networks. To that end, we conducted EEG source reconstruction on spindle epochs in both cortical and subcortical regions using novel deep-source localization techniques. Coherence-based metrics were adopted to estimate functional connectivity between cortical and subcortical structures over specific frequency bands. Our findings not only confirm the critical and functional role of NREM-stage2 sleep spindles in motor skill consolidation, but provide first-time evidence that spindle oscillations [11–17 Hz] may be involved in sleep-dependent motor memory consolidation by locally reactivating and functionally binding specific task-relevant cortical and subcortical regions within networks including the hippocampus, putamen, thalamus and motor-related cortical regions.

The role of laminin receptors in colorectal cancer (CRC) is the subject of ongoing research. Histopathological studies have suggested that the 67 kDa laminin receptor (67LR) is involved in the carcinogenesis of various malignancies, including CRC. However, the exact composition and nature of 67LR have been a source of confusion for many years. A recent study from our group reported that the 37 kDa form of RPSA participates as a laminin receptor renamed the RPSA-containing laminin receptor (RCLR) but is not the precursor form of the 67LR since the 67 kDa protein associated with 67LR corresponds to the 67 kDa elastin-binding protein (67EBP), which also acts as a laminin receptor. The present study aims to analyze the distinct expression patterns of these two laminin receptor components in CRC. Expressions of RCLR and 67EBP were analyzed in CRC tissues using Western blot and quantitative RT-PCR analyses. The primary colorectal adenocarcinoma tissues and corresponding resection margins showed an overexpression of both RPSA and 67EBP at the protein level in the CRC tissues. An analysis of the publicly available CRC datasets confirmed the overexpression of RPSA and 67EBP in CRC tissues. In conclusion, the elevated expression of these two non-integrin laminin receptors in CRC lesions suggests their critical roles in colorectal carcinogenesis and emphasizes their potential usefulness as tissue biomarkers.

Determining the prevalence and characteristics of individuals susceptible to present with obstructive sleep apnea (OSA) is essential for developing targeted and efficient prevention and screening strategies. We included 27,210 participants aged ≥45 years old (50.3% women) from the Canadian Longitudinal Study on Aging. Using the STOP questionnaire combined to the percentage of body fat (%BF), we estimated the prevalence of individuals at high-risk for OSA in a sex and age-specific manner, and tested the relation with comorbidities, menopause and systemic inflammation. The prevalence was 17.5%, and was lower in women (13.1%) than in men (21.9%). A high level of high-sensitivity C-reactive protein was the strongest factor associated with OSA risk and this association was 1.3–2.3 times higher in women than in men. OSA risk increased with age, cardiovascular diseases, diabetes mellitus, anxio-depressive symptoms, asthma and arthritis. In women, post-menopausal status was associated with a high OSA risk. Nearly 1 adult out of 5 older than 45 is at risk for OSA in Canada. Comorbidities, menopause and systemic inflammation, more than age, explain increased OSA prevalence. Considering this high prevalence and associations with medical and mental comorbidities, health care practitioners should incorporate systematic OSA screening in their clinical procedures.

The PTEN phosphatase acts on phosphatidylinositol 3,4,5-triphosphates resulting from phosphatidylinositol 3-kinase (PI3K) activation. PTEN expression has been shown to be decreased in colorectal cancer. Little is known however as to the specific cellular role of PTEN in human intestinal epithelial cells. The aim of this study was to investigate the role of PTEN in human colorectal cancer cells. Caco-2/15, HCT116 and CT26 cells were infected with recombinant lentiviruses expressing a shRNA specifically designed to knock-down PTEN. The impact of PTEN downregulation was analyzed on cell polarization and differentiation, intercellular junction integrity (expression of cell-cell adhesion proteins, barrier function), migration (wound assay), invasion (matrigel-coated transwells) and on tumor and metastasis formation in mice. Electron microscopy analysis showed that lentiviral infection of PTEN shRNA significantly inhibited Caco-2/15 cell polarization, functional differentiation and brush border development. A strong reduction in claudin 1, 3, 4 and 8 was also observed as well as a decrease in transepithelial resistance. Loss of PTEN expression increased the spreading, migration and invasion capacities of colorectal cancer cells in vitro. PTEN downregulation also increased tumor size following subcutaneous injection of colorectal cancer cells in nude mice. Finally, loss of PTEN expression in HCT116 and CT26, but not in Caco-2/15, led to an increase in their metastatic potential following tail-vein injections in mice. Altogether, these results indicate that PTEN controls cellular polarity, establishment of cell-cell junctions, paracellular permeability, migration and tumorigenic/metastatic potential of human colorectal cancer cells.

Motor memory consolidation is thought to depend on sleep-dependent reactivation of brain areas recruited during learning. However, up to this point, there has been no direct evidence to support this assertion in humans, and the physiological processes supporting such reactivation are unknown. Here, simultaneous electroencephalographic and functional magnetic resonance imaging (EEG-fMRI) recordings were conducted during post-learning sleep to directly investigate the spindle-related reactivation of a memory trace formed during motor sequence learning (MSL), and its relationship to overnight enhancement in performance (reflecting consolidation). We show that brain regions within the striato-cerebello-cortical network recruited during training on the MSL task, and in particular the striatum, were also activated during sleep, time-locked to spindles. Interestingly, the consolidated trace in the striatum was not simply strengthened, but was transformed/reorganized from rostrodorsal (associative) to caudoventral (sensorimotor) subregions. Moreover, the degree of the reactivation was correlated with overnight improvements in performance. Altogether, the present findings demonstrate that striatal reactivation linked to sleep spindles in the post-learning night, is related to motor memory consolidation.

This study investigated the prospective links between sleep in infancy and preschoolers' cognitive performance. Mothers of 65 infants completed a sleep diary when infants were aged 1 year, and children completed two subscales of the Wechsler Preschool and Primary Scale of Intelligence at 4 years, indexing general cognitive ability and complex executive functioning. Consistent with hypotheses, children getting higher proportions of their sleep at night as infants were found to perform better on executive functions, but did not show better general cognition. Relations held after controlling for family socioeconomic status and prior cognitive functioning. These findings suggest that the special importance of sleep for higher order cognition, documented among adults, may appear very early in life.

Memory consolidation can be enhanced during sleep using targeted memory reactivation (TMR) and closed-loop (CL) acoustic stimulation on the up-phase of slow oscillations (SOs). Here, we test whether applying TMR at specific phases of the SOs (up vs. down vs. no reactivation) can influence the behavioral and neural correlates of motor memory consolidation in healthy young adults. Results show that up- (as compared to down-) state cueing results in greater performance improvement. Sleep electrophysiological data indicate that up- (as compared to down-) stimulated SOs exhibits higher amplitude and greater peak-nested sigma power. Task-related functional magnetic resonance images reveal that up-state cueing strengthens activity in - and segregation of - striato-motor and hippocampal networks; and that these modulations are related to the beneficial effect of TMR on sleep features and performance. Overall, these findings highlight the potential of CL-TMR to induce phase-specific modulations of motor performance, sleep oscillations and brain responses during motor memory consolidation. Here, the authors show that reactivating motor memories during sleep at moments of high (vs. low) neuronal excitability (up vs. down phases of slow oscillations) enhances their consolidation. Up-reactivation strengthens sleep markers of plasticity and the neural responses supporting memory consolidation.

Chronotype is shaped by the complex interplay of endogenous and exogenous factors. This time-enduring trait ties into societal behaviors and is linked to psychiatric and metabolic conditions. Despite its multifaceted nature, prior research has treated chronotype as a monolithic trait across the population, risking overlooking substantial heterogeneity in neural and behavioral fingerprints. To uncover hidden subgroups, we develop a supervised pattern-learning framework integrating three complementary brain-imaging modalities with deep behavioral and health profiling from 27,030 UK Biobank participants. We identify five distinct, biologically valid chronotype subtypes. Each demonstrates unique patterns across brain, behavioral and health profiles. External validation in 10,550 US children from the ABCD Study cohort reveals reversed age distributions and replicates sex-associated brain-behavioral patterns, suggesting that potential divergences between chronotype traits observed throughout adulthood may begin to emerge early in life. These findings highlight underappreciated sources of population variation that echo the rhythm of people’s inner clock. Combining multiomic datasets from adolescent and middle-aged-to-older population cohorts with a purposefully devised analytical framework, we revealed substantial heterogeneity in brain-chronotype-behavior patterns and their complex interactions with everyday life.