Brain Function Research Articles (Page 1)

Coaching is a well-established practice. Yet given the many different approaches bearing the label coaching, all claiming to be at least as effective as the others, scholars and practitioners are left struggling to come up with a common conceptual framework. Here I propose that coaching approaches are united by a single learning mechanism to which we are all subject. Predictive Processing (PP) is an emerging theory of brain functioning which explains how humans learn by making and correcting ‘prediction errors.’ Since all coaching involves learning, working with this mechanism, whether explicitly or implicitly, is a key element in how coaching helps clients to achieve their aims. By expanding the common ground for dialogue between followers of different traditions, I hope it can contribute to the development of a more coherent theoretical foundation for coaching. By explaining the principles of PP and how they are reflected in models of learning and coaching practice, I also hope to show how they can help refine and deepen practitioners’ understanding of how coaching works.

Autism Spectrum Disorder (ASD) involves complex neurodevelopmental interactions between the gastrointestinal tract, gut microbiota, and brain function. Growing evidences implicated that bidirectional microbiota-gut-brain axis signaling in ASD pathophysiology. This study examines how Lactobacillus acidophilus (ATCC-4356) alters behavioral phenotypes in a valproic acid-induced maternal immune activation (MIA) mouse model of autism. The MIA model was intraperitoneally injected with valproic acid, while controls were intraperitoneally injected with saline. Behavioral testing showed that repetitive, stereotyped, anxiety-like, and social behaviors were significantly improved (P < 0.05) after L. acidophilus (ATCC-4356) intragastric administration for seven weeks. Western blot analysis demonstrated that tight junction proteins (Claudin 1, Claudin 3, Occludin, and ZO) were highly expressed in the L. acidophilus (ATCC-4356) group versus the autism model (P < 0.05), suggesting enhanced intestinal barrier integrity. Inflammatory factor concentrations in both colon and hippocampus were markedly reduced in the L. acidophilus (ATCC-4356) group (P < 0.05). Gut microbiota sequencing showed significant increases of microbial diversity and richness in the L. acidophilus (ATCC-4356) group (P < 0.05). Hippocampal immunofluorescence revealed higher NeuN-, Ki67-, and BrdU-positive cell counts in the L. acidophilus (ATCC-4356) group (P < 0.05). Results suggest that L. acidophilus (ATCC-4356) ameliorates autistic-like behaviors, potentially through modulation of intestinal barrier function. Furthermore, results showed that therapeutic efficacy was reduced by L. acidophilus (ATCC-4356) in autism after antibiotic-induced dysbiosis of the intestinal microbiota In this paper, the results showed that L. acidophilus (ATCC-4356) improves autism-like behaviors by modulating gut barrier function.

Long-term (>7-year) neurodevelopmental safety assessment of genetically modified (Cry1Ab/Cry2Aj and EPSPS) maize in cynomolgus monkeys: A multimodal MRI study across two generations.

Organoids derived from stem cells have significantly advanced disease modeling, particularly in neurodegenerative disorders, while advancing personalized and regenerative medicine. These three-dimensional structures reproduce key aspects of human brain organization and functionality, while remaining simplified models that do not yet recapitulate full neural circuitry or disease progression, providing an improved platform for studying disease mechanisms, drug responses, and potential therapeutic strategies. This review explores the methodologies used in organoid development, including the differentiation of stem cells and culture techniques that enable the formation of self-organizing tissues. Organoids have been successfully used to model key cellular and molecular aspects of neurodegenerative diseases such as Alzheimer’s and Parkinson’s, offering insights into early disease mechanisms and potential novel treatment strategies. Key findings highlight that organoids provide more physiologically relevant data than traditional two-dimensional cultures and animal models, making them valuable tools for preclinical research and personalized treatment approaches. However, challenges remain, including variability in organoid generation, lack of vascularization, and difficulties in large-scale production for clinical applications. For the effective integration of organoids into biomedical and clinical applications, future research should prioritize improving reproducibility, standardization, and vascularization methods. Addressing these limitations will enhance their translational potential, leading to more effective treatments for neurodegenerative disorders and broader applications in precision medicine.

Altered Local Spontaneous Brain Activity in Cervical Spondylotic Myelopathy: A Meta-analysis.

Background: The endocannabinoid system (ECs) with its receptors and ligands is a complex cell-signalling system widely present in the nervous system and in the gastrointestinal tract. The ECs regulates inflammatory responses and intestinal homeostasis through its interactions with the gut microbiota, ultimately influencing brain function both indirectly, via gut-derived circulating factors, and directly, through vagus nerve signalling. Increasing evidence points to a role for the ECs in chronic migraine. The aim of this study was to assess whether gut dysbiosis is associated with alterations in the ECs, both centrally and peripherally, in a chronic migraine-like animal model induced by repeated nitroglycerin (NTG) administration. Methods: Adult male Sprague-Dawley rats were treated with NTG (5 mg/kg i.p.) or vehicle every two days over nine days (5 total injections). On day nine, four hours after the last administration of NTG or vehicle, rats were tested for migraine-like hyperalgesia (orofacial formalin test). The intestine and trigeminal ganglion were collected to assess the gene expression of ECs components using real-time PCR. Fecal 16S ribosomal RNA gene sequencing was used to assess alterations in the gut flora. Results: Chronic NTG administration significantly increased face rubbing time during phase II of the orofacial formalin test, confirming the development of trigeminal hyperalgesia. Gut microbiota analysis revealed significant differences in beta-diversity between NTG-treated and vehicle groups, confirming an alteration in the microbial population. Furthermore, analysis of intestinal gene expression showed a significant decrease in monoacylglycerol lipase (MAGL) mRNA expression, with no changes observed in the mRNA expression of fatty acid amide hydrolase, N-acylethanolamine acid amidase, N-acyl phosphatidylcholine phospholipase D, cannabinoid receptor-1, and cannabinoid receptor-2. Accordingly, reduced MAGL mRNA expression was also detected in the trigeminal ganglion of NTG-treated rats compared to the vehicle group. Conclusion: These findings suggest that microbiota dysbiosis associated with trigeminal hyperalgesia may be linked to altered 2-arachidonoylglycerol metabolism, suggesting a potential role for the gut-brain-endocannabinoid axis in migraine-related pain.

Background and objectives: Exerkines are signalling factors that are released from organs throughout the body during physical exercise (El-Sayes et al., 2019). Some of these exerkines are thought to contribute to the well-documented benefits of exercise on brain health and cognitive function, potentially delaying age-related cognitive decline (Erickson et al., 2011). However, research is still far from establishing a mechanism-based, evidence-driven exercise programme to prevent such decline. To date, most studies have focused on endurance training, leaving other training modalities underexplored. Moreover, few studies have simultaneously examined exercise-induced effects on blood, brain, and cognitive domains, limiting more holistic understanding of the underlying mechanisms. Research has also primarily involved healthy adults, whereas older adults at risk of Mild Cognitive Impairment (MCI) are less frequently studied. Importantly, the effects of exercise on cognition have never been investigated in persons with Spinal Cord Injury (SCI), a population with an elevated risk of age-related cognitive decline and dementia. The primary objective of the dissertation was therefore to gain a more comprehensive understanding of the mechanisms underlying the beneficial effects of exercise training, specifically resistance exercise in older adults and Neuromuscular Electrical Stimulation (NMES) in individuals with SCI, on brain health and cognitive function, with a particular focus on the role of exerkines in (exercise-induced) neuroplasticity. Methods: Eleven studies were conducted. Study 1 was a literature review describing exerkine release following acute and chronic endurance or resistance exercise and their effects on neuroplasticity via long-term synaptic potentiation. Study 2 summarised the findings from transcriptome and secretome studies identifying muscle-derived exerkines (myokines). Studies 3 and 4 were cross-sectional studies in older adults (n = 74) investigating the relationships between participant characteristics, blood (inflammatory and neurotrophic) and brain biomarkers (neurometabolites, regional grey matter volumes), and cognitive function. Studies 5–8 evaluated the effect of a single bout (n = 37) and a 12-week resistance exercise programme (n = 74) on blood and brain biomarkers and cognitive function in older adults. Studies 6 and 7 further compared outcomes between cognitively healthy older adults and those at elevated risk of MCI (based on the Montreal Cognitive Assessment). Study 9 systematically reviewed evidence on the effects of exercise interventions on cognitive performance in individuals with SCI and highlighted factors underlying their elevated risk of cognitive decline. Study 10 tested the effect of a single bout of NMES on exerkines and cognitive performance in persons with SCI. Study 11 described the protocol of a 12-week NMES intervention in individuals with SCI to examine the effect on exerkines and cognitive outcomes. Results: Study 1 identified 16 exerkines with known (in)direct effects on long-term synaptic potentiation. Study 2 reported 1,126 putative myokines, most with still unknown effects on the brain and body. Study 3 found associations between the circulating inflammatory marker kynurenine and signs of neuroinflammation and neurodegeneration in older adults. Study 4 showed that older adults with normal-to-slightly-elevated body weight and greater handgrip strength maintained larger brain volumes. Study 5 demonstrated improved working memory performance in older adults immediately after a single session of resistance exercise training compared to control group. Study 6 suggested hippocampal volume preservation over time in the resistance exercise group, and Study 7 revealed executive function improvements in older adults at elevated risk of MCI after 12 weeks of resistance training compared with control group. Study 8 demonstrated neurometabolic changes in older adults who contracted COVID-19 during participation. Study 9 confirmed that no prior studies have investigated exercise effects on cognitive function in individuals with SCI. Study 10 found increases in lactate levels, but no changes in cognitive performance after a single NMES session in persons with SCI. Study 11 described the design for a future 12-week NMES intervention study for individuals with SCI. Conclusions: The dissertation advances the understanding of exercise effects on brain health and cognition in older adults and individuals with SCI, providing a neurobiological basis for future research. Kynurenine levels, handgrip strength, and a healthy body weight emerged as potential biomarkers of brain health for older adults. The findings underscore the importance of monitoring cognitive functioning in persons with SCI. Although further research is needed to clarify the effect of different exercise modalities across populations with varying cognitive risk profiles, the present evidence reinforces the notion that physical exercise benefits brain function. A multimodal, enjoyable, and sustainable exercise programme maintained throughout life is likely to be the most effective strategy to mitigate or delay age-related cognitive decline. Keywords: aging, cognition, myokines, exercise, spinal cord injury

Minimal hepatic encephalopathy (MHE) is the initial stage of hepatic encephalopathy (HE), MHE patients have associated with widespread neuro-psychological impairment. Liver transplantation (LT) can restore metabolic abnormalities but the mechanisms are unclear. This study aimed to longitudinally evaluate brain function alteration in MHE patients one month after LT and their correlation with cognitive changes by using resting-state functional magnetic resonance imaging (rs-fMRI). Rs-fMRI data was collected from 32 healthy controls and 27 MHE before and 1 month after LT. Between-group comparisons of demographic data and neuropsychological scores were analyzed using SPSS 25.0. Functional imaging data were analyzed using RESTplus and SPM12 software based on MATLAB 2017b. Gender, age, and years of education were used as covariates to obtain low-frequency fluctuationd (ALFF) and dynamic low-frequency fluctuation (dALFF) dindices. Correlation analyses were performed to explore the relationship between the change of ALFF and dALFF with the change of clinical indexes pre- and post-LT. Compared to controls, ALFF values increased in the Left Cerebelum 8, right orbital part of the inferior frontal gyrus (ORBinf), right superior occipital gyrus (SOG) and decreased in right PreCG and left middle frontal gyrus (MFG) in patients post-LT; dALFF values increased in the right temporal pole and middle temporal gyrus (TPOmid), right ORBinf, left caudate nucleus (CAU), right SOG and decreased in left PreCG, left PCUN, left ANG, left SMA and left MFG in patients post-LT. Compared to pre-LT, ALFF values of post-LT patients increased in the right calcarine fissure and surrounding cortex (CAL), right MOG and decreased in right cerebelum 8, left PCUN; dALFF values of post-LT patients decreased in right thalamus (THA), left posterior cingulate gyrus (PCG) and left MFG. The changes of ALFF in the left PCUN, right CAL and right MOG were correlated with change of digit symbol test (DST) scores ( P &amp;lt; 0.05). In summary, this study not only showcases the potential of ALFF/dALFF algorithms for assessing alterations in spontaneous neural activity in MHE, but also provides new insights into the altered brain functions in MHE patients 1 month after LT, which may facilitate the elucidation of elucidation of mechanisms underlying cognitive restoration post-LT in MHE patients.

Neuroscience has advanced rapidly over the past century by applying reductionist methods to dissect brain function at molecular, cellular, and circuit levels, primarily in animal models. While this approach has generated extraordinary insights, the field now faces an epistemological bottleneck: efforts to build holistic models of human cognition from fragmented reductionist data are failing to capture the complexity of real-world brain function. Current translational pathways are dominated by a clinical mission-using dysfunction to model normal function-which limits ecological validity and reinforces blind spots. We argue that neuroscience must broaden its ontological mission beyond treatment of DSM-defined disorders to include functional misalignments and productivity in everyday life, encompassing education, workplaces, and social contexts. To achieve this, we propose the concept of behavioral "wind tunnels," an analogy to the facilities that transformed aerodynamics. Like wind tunnels, such environments would provide a controlled yet naturalistic middle ground between laboratory reductionism and the uncontrolled complexity of real-world settings. They would enable scalable capture of cognitive traits and states across wide populations, long time horizons, and multiple functional dimensions, yielding ecologically valid feedback loops essential for both theory and application. Embedding neuroscience into real-world contexts would align the field with pressing societal needs-optimizing human skills in an AI-disrupted economy, fostering resilience to global crises, and advancing brain health as an economic and societal asset. Just as wind tunnels transformed aviation from theory to reliable practice, neuroscience must now adopt analogous infrastructures to realize its full potential for humanity.

Cerebrospinal fluid (CSF) flow within perivascular routes (PVS) is essential for maintaining brain health and function. This flow is a part of the glymphatic system, which clears waste products and metabolic byproducts from the brain. The PVS boundaries consist of a non-permeable arterial vessel wall and neural tissue. The arterial vessel peristalsis and the elasticity of the neural tissue are responsible for generating the CSF flow. This article examines the effect of a transverse magnetostatic field and pertinent physiological conditions on CSF flow. It specifically considers the impact of brain elasticity and porosity at the neuroglial layers, arterial wall curvature, and the peristalsis amplitude. The effective Navier–Stokes governing equations describe the peristalsis of CSF flow subjected to a magnetostatic field. The perturbation strategy is utilized to address the governing equations. This leads to a set of equations describing CSF stream-direction velocity, pressure gradient, and neural tissue deformation. The graphical outcomes highlight the significant influence of a range of physiological and flow factors on the behavior of CSF. The key parameters encompass neural tissue porosity and stiffness, neuroglial layer deformation, magnetostatic field strength, and arterial wall curvature. The results reveal that enhancing the magnetostatic field intensity reduces CSF pressure distribution, stream-direction velocity, and arterial deformation. This study is highly significant due to its implications for the development and advancement of different neurological disorders for instance Alzheimer’s disease, meningeal inflammation, neurotrauma, and hemorrhagic stroke.

Gap junctions (GJs) are intercellular channels that mediate electrical signals and transfer of small molecules. They are crucial for brain, heart, and other organ functions. While molecular structures of purified homomeric GJs are available, information of in situ structures is lacking. In vivo, GJs can form heteromers with different functionalities and may associate with other proteins. Here, we analyzed Caenorhabditis elegans GJs by cryo–electron tomography and subtomogram averaging. We observed hexagonal arrays of GJs at cellular junctions in primary embryonal cells that displayed distinct wide and narrow conformations. Moreover, we found a cap-like, cytosolic protein assembly enclosing the channel pore. We propose that the cap is formed by the stomatin UNC-1, known to interact with UNC-9 innexins. This is corroborated by matching AlphaFold3 models of UNC-1 multimers with our subtomogram average structure; by expressing GFP-tagged UNC-1, leading to cap structures with additional density; and by coarse-grained MD simulations. UNC-1/stomatin rings may affect GJ formation or functions, possibly beyond nematodes.

Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique where electrodes applied to the scalp deliver electrical currents and modify the neuronal cell environment. Research shows that tDCS can improve cognitive functions in older adults by modulating brain function via delivered increasing current in the brain. We aimed to investigate the impact of individual tissue identities on the delivered current density value in the brain. Six models (M1–M6) were created for analysis. M6 was assigned as the reference model, incorporating the six most used tissue types (i.e., white matter, grey matter, CSF, skin, and bone). The M2–M5 models were compared to the M6 reference model, with each model incorporating one additional tissue type to assess its specific contribution to current density (J) (i.e., blood, eye, fat, and separating bone into cancellous and cortical bone, respectively). M1 included all eleven tissues tested. Magnetic resonance images (MRIs) were acquired in four older adults (2M, 2F, M_age = 73 years) and were segmented into each of the six models using a combination of automatic and manual tissue segmentation. Electrodes were placed using a F3- F4 montage, with a 2mA input current. Each tissue was assigned unique conductivity values and electric fields were generated using the COMSOL AC/DC module. The white matter and grey matter regions were isolated and combined to compute J values in the brain (Jbrain). Jbrain in M1-M5 was compared to M6 using a Welch’s t-test in RStudio. We found that, among the six models, M1 (median Jbrain = 0.020381 Am-2), M4 (median Jbrain = 0.018377 Am-2), and M5 (median Jbrain = 0.015608 Am-2) were statistically significantly (p-value &lt;0.001) different from the reference model M6. This research offers an understanding of how various head tissues contribute to the current density in the brain, aiding in the planning of future tDCS modeling using these techniques.

Abstract Background Obesity is recognized as a pathological condition characterized by excess body fat, which may be associated with impaired brain function, particularly with a reduction in attentional capacity. Fibromyalgia, a chronic rheumatic disorder, is marked by musculoskeletal pain, fatigue and sleep disturbances. When both obesity and fibromyalgia coexist, they worsen rheumatic symptoms and may contribute to cognitive decline. This study aimed to evaluate the association between cognitive function, body composition, and anthropometric indices in women with fibromyalgia. Results Exploratory, cross-sectional, correlational pilot study in 18 women with fibromyalgia. Sociodemographic and clinical characteristics, body composition, cognitive function, and variables related to mental health were examined. Body mass index, waist-to-hip ratio, and waist-to-height ratio were calculated. Spearman test was used to evaluate the correlation between body composition variables and cognitive function. The mean age was 44.4 ± 10.7 years. 83.3% were overweight, 35.3% had a high percentage of fat, and 61.1% had a high cardiovascular risk. Regarding cognitive function, 72.2% presented probable cognitive impairment. Delayed recall was the only domain significantly correlated with body composition, showing inverse associations with fat mass ( r = − 0.62; p = 0.004) and cardiovascular risk ( r = − 0.49; p = 0.022). Conclusion Women diagnosed with fibromyalgia face significant cognitive impairment, as well as elevated levels of stress, anxiety, and depression associated with a state of excess malnutrition. Further research is suggested to validate and extend these findings and explore specific therapeutic interventions based on individualized care.

This article examines how digital technology affects the thinking and emotional well-being of young people. Spending too much time on screens can make it harder to concentrate, remember important information, get enough sleep, and manage emotions. Research shows that frequent use of smartphones and social media leads to serious problems known as digital dementia and brain rot. These habits can change brain function, cause unhealthy behaviors, and mental disorders. The negative effects can be reduced by setting limits on device use and encouraging controlled usage. Simple steps such as putting phones away during meals, reading printed books, and spending more time outdoors have been shown to have positive impacts on health. Taking regular breaks from digital content also helps the mind stay clear. The complex problem of the digital era can only be solved with collective action. All interested parties should cooperate on the policies and guidelines for using digital tools to protect mental health in the long run.

Neurodevelopmental disorders that cause cognitive, behavioural or motor impairments affect around 15% of children and adolescents worldwide1, with diagnoses of profound autism and attention deficit hyperactivity disorder increasing in the USA and contributing to amajor economic burden2,3. Yet the origins and mechanisms of these conditions remain poorly understood, limiting progress in therapies. Comprehensive cell atlases of the developing human brain, alongside those of model organisms such as mice and non-human primates, are now providing high-resolution measures of gene expression, cell-type abundance and spatial distribution. In this Perspective, we highlight recent studies that have identified novel developmental cell populations, revealed conserved and divergent patterns of cell genesis, migration and maturation across species, and begun testing hypotheses that link them to processes ranging from transcriptional control of cell fate specification to the emergence of complex behaviours. We present remaining conceptual and technical challenges and provide an outlook on how further studies of human and mammalian brain development can empower a deeper understanding of neurodevelopmental and neuropsychiatric disorders. Future efforts expanding to additional developmental stages, including adolescence, as well as whole-brain, multimodal and cross-species integration, will yield new insights into how development shapes the brain. These atlases promise to serve as essential references for unravelling mechanisms of brain function and disease vulnerability, and for advancing precision medicine.

BackgroundIron overload plays a role in the pathogenesis of neurodegenerative disorders by inducing oxidative injury in the brain. Centella asiatica (L.) Urb. It is a medicinal plant with neuroprotective effects that exhibits antioxidant and anti-inflammatory activities. A standardized extract of C. asiatica (ECa 233) has high concentrations of the bioactive compounds madecassoside and asiaticoside. It may have potential for use in iron overload conditions.ObjectivesThis study aimed to investigate the effects of ECa 233 on iron-induced brain injury, memory deficits, and impaired locomotor activity in 12-month-old wild-type (WT) and β-thalassemia (β-globin knockout, BKO) mice with iron overload.MethodsWT and BKO mice were intraperitoneally (i.p.) injected with 100 mg of iron, followed by i.p. injection of 20 mg/kg body weight of ECa 233 for 10 days. Iron accumulation and injury in the brain were evaluated via hematoxylin and eosin (H&E) and Prussian blue staining. The Morris water maze (MWM) and open field tests were performed to evaluate spatial learning and memory and locomotor activity, respectively.ResultsAging BKO mice resulted in spontaneous iron accumulation in the brain and poor performance in the MWM test. Iron overload significantly increased brain iron content and worsened brain injury, locomotor activity, and performance in the MWM test in both WT and BKO mice. Treatment with ECa 233 significantly decreased iron accumulation in the brain and reversed brain damage in WT and BKO mice to the same extent. In addition, ECa 233 improved iron-induced memory deficits in WT mice and locomotor activity in iron-overloaded WT and BKO mice.ConclusionThese results suggest that the beneficial effect of ECa 233 may be partially due to decreased iron accumulation in the brain. ECa 233 may be used as an adjuvant with an iron chelator to prevent iron-induced neurodegenerative complications in individuals with β-thalassemia.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12906-025-05145-w.

Neuroplasticity in childhood is a key mechanism underlying the formation of brain structure and function during early ontogenesis. This article synthesizes current scientific knowledge on the biological foundations, critical periods, influencing factors, and clinical relevance of neuroplastic processes in children. An analysis of studies published over the past 5–7 years highlights the principal pathways of neuronal network formation under both typical development and in the context of developmental disorders, as well as the potential of early interventions to stimulate plastic changes. Aim: to summarize recent findings on neuroplastic processes in childhood, with particular emphasis on their biological mechanisms, the impact of environmental factors, and their significance for clinical practice. Materials and Methods. This review is based on 26 scientific publications published between 2018 and 2024. Sources were retrieved from international databases (PubMed, Scopus, Web of Science) using keywords such as neuroplasticity, brain development, children, early intervention, and functional reorganization. The analysis encompassed experimental, review, and longitudinal studies, employing critical evaluation of neuroimaging, clinical-physiological, and behavioral research on the developing brain. Results. Neuroplasticity reaches its peak during early childhood, characterized by intensive synaptogenesis, myelination, the establishment of inter-neuronal connections, and the capacity for functional reorganization following injury. Positive modulators include sensory enrichment, cognitive stimulation, social interaction, and physical activity, whereas adverse experiences (e.g., deprivation, stress, isolation) exert long-term inhibitory effects on brain development. Evidence also demonstrates a high compensatory potential in the child’s brain, facilitated by the activation of alternative neural pathways in cases of organic damage. Conclusion. Childhood neuroplasticity is a critical determinant of cognitive, speech, and motor development, as well as the success of interventions for neurodevelopmental disorders. Optimal outcomes depend on early identification of a child’s needs and the implementation of personalized developmental support strategies. Future research should prioritize individual differences in plasticity and the development of targeted protocols to enhance neuroplasticity in both clinical and educational settings.

Sleep is a fundamental physiological process essential for maintaining both physical and mental health. While significant advances have been made in understanding the central nervous system mechanisms that regulate sleep-wake cycles, emerging evidence reveals the crucial role of peripheral organs, particularly the digestive system, in modulating brain function and behavior through the microbiota-gut-brain axis. This bidirectional communication network between the gut and the central nervous system directly and indirectly impacts sleep regulation. Disruptions in gut microbiota composition are closely linked to sleep disturbances, and alterations in the microbiota-gut-brain axis have been observed in several sleep disorders and illnesses with comorbid sleep disturbances. This review synthesizes current insights into the interplay between gut microbiota and sleep-wake regulation, highlighting potential routes of the microbiota-gut-brain axis in sleep and gut microbiome interactions and their health implications. Modulating gut microbiota may present a promising strategy for developing novel therapeutic approaches to address sleep disorders.

Human neural networks of interconnected neurons have evolved to be remarkably efficient and are capable of learning and memory through the brain's synaptic plasticity, including short-term plasticity (STP), and long-term potentiation (LTP) and depression (LTD). These activity-dependent mechanisms induce changes in synaptic efficiency over both transient and extended timescales. Understanding the molecular basis of learning and memory is central to deciphering brain function and advancing therapeutics for neurodegenerative diseases. Here, we report that lipid bilayers with embedded gramicidin A ion channels can structurally reorganize when interrogated using a neurologically inspired electrical stimulation protocol, adopting metastable structures with enhanced STP response and emergent LTP or LTD. Specifically, voltage-induced electrocompression is found to restructure membranes, driving them into nonequilibrium steady states with enhanced stability and increased ionic conductivity, leading to stronger and persistent membrane ion conductance. These results show how membrane restructuring and emergent complexity may regulate synaptic plasticity at the molecular level.

Stress significantly impacts brain function and is a major contributor to major depressive disorder. This study explores the role of long noncoding RNAs (lncRNAs) in stress-induced chromatin remodeling and gene regulation, particularly in the context of glucocorticoid receptor (GR) activation, a hallmark of stress-related disorders. Using a cellular model, GR activation regulated 79 lncRNAs: 44 upregulated and 35 downregulated. Chromosome-wise analyses of lncRNA regulation revealed complex patterns, with specific chromosomes, chr1 and chr15, showing a higher prevalence of downregulated genes, while chr11 and chr12 exhibited upregulated genes, indicating the differential roles of lncRNAs in gene silencing and activation. The differentially regulated lncRNAs were further classified into intergenic, overlap_antisense and overlap_sense, revealing their diverse roles in regulating gene expression. An immunoprecipitated ribonucleoprotein assay followed by sequencing confirmed the interaction of lncRNAs with a histone methyltransferase primarily targeting histone H3 lysine 27 (H3K27), with 87 lncRNAs enriched in the pull-down group, and 51 enriched in the EZH2 pull-down, a part of Polycomb Repressive Complex 2 (PRC2), linking these lncRNAs to PRC2-mediated chromatin repression. An integrative analysis revealed an inverse correlation between specific lncRNAs and the transcriptional activity of proximal genes, supporting the role of lncRNAs in gene silencing. Gene ontology of suppressed genes highlighted enrichment in functions related to neuronal death and synaptic transmission. Altogether, our study demonstrates that lncRNAs, particularly those interacting with PRC2, may serve as potential mediators of stress-induced neuronal changes by influencing chromatin accessibility, and potentially highlight their roles in stress-related disorders.