Dr. Zaw Myo Hein is an Assistant Professor of Anatomy at the College of Medicine, Ajman University. He earned his MBBS from the University of Medicine-2, Yangon, Myanmar, and initially practiced as a physician in various hospitals. Dr. Hein also served as a faculty member in the Department of Anatomy at the University of Medicine-1, Yangon, Myanmar. He completed his PhD in Neuroscience at Mahidol University, Thailand, with a focus on neurotoxicity, neuroinflammation, cognitive function, and the neuroprotective potential of melatonin and aquaporins in the brain. His research has earned him several grants and accolades, including a prestigious PhD scholarship from the Norwegian Programme for Capacity Development. A proactive and dynamic scholar, Dr. Hein has collaborated with esteemed institutions such as the Albert Einstein College of Medicine, New York, and the University of Oslo. He has presented his groundbreaking research at major international conferences, including the IBRO World Congress, the Society for Neuroscience Conference, and the American Association for Anatomy Conference.
Abstract Artificial intelligence (AI) and machine learning (ML), especially deep learning, have profoundly transformed biology by enabling precise interpretation of complex genomic and proteomic data. This review presents a comprehensive overview of cutting-edge AI methodologies spanning from foundational neural networks to advanced transformer architectures and large language models (LLMs). These tools have revolutionized our ability to predict gene function, identify genetic variants, and accurately determine protein structures and interactions, exemplified by landmark milestones such as AlphaFold and DeepBind. We elaborate on the synergistic integration of genomics and protein structure prediction through AI, highlighting recent breakthroughs in generative models capable of designing novel proteins and genomic sequences at unprecedented scale and accuracy. Furthermore, the fusion of multi-omics data using graph neural networks and hybrid AI frameworks has provided nuanced insights into cellular heterogeneity and disease mechanisms, propelling personalized medicine and drug discovery. This review also discusses ongoing challenges including data quality, model interpretability, ethical concerns, and computational demands. By synthesizing current progress and emerging frontiers, we provide insights to guide researchers in harnessing AI’s transformative power across the biological spectrum from genes to functional proteins. Keywords: artificial intelligence; genomics; protein structure prediction; deep learning; precision medicine; convolutional neural networks; multi-omics integration
Whole-body vibration therapy (WBVT) is increasingly recognized as an alternative exercise modality with established benefits for musculoskeletal and cardiovascular health. Its effects on cognitive performance and autonomic regulation in healthy young adults, however, remain unclear. This within-subject study investigated whether acute WBVT influences executive function and heart rate variability (HRV). Thirty-six healthy volunteers (aged 18–25 years) completed two testing sessions separated by 7 days: a baseline (no vibration) session and a single 10-min WBVT session performed in a standing posture. Cognitive performance was assessed immediately after each session using a modified Stroop test, and electrocardiographic recordings were analyzed for HRV indices, including stress index, low-frequency (LF) and high-frequency (HF) power, LF/HF ratio, and mean heart rate. Compared with baseline, WBVT was associated with faster mean reaction times for congruent and incongruent Stroop stimuli (all p < 0.001) without changes in response accuracy. The stress index increased during the Stroop task relative to baseline (p = 0.052) and returned toward baseline following WBVT, whereas LF, HF, the LF/HF ratio, and total power showed no statistically significant changes. In this cohort, acute WBVT was associated with improved processing speed without measurable alterations in standard HRV metrics. These preliminary findings suggest that WBVT may transiently facilitate attentional processing in healthy young adults, but controlled trials with sham conditions and mechanistic measures are needed to confirm and contextualize these effects. Keywords: whole body vibration, therapy, cognitive function, heart rate variability, Stroop Test, executive function
Introduction Understanding medical students' perceptions of anatomy teaching resources is crucial for developing effective and engaging educational strategies that enhance long-term knowledge retention. This study examined students’ preferences for various gross anatomy and histology learning resources and evaluated their perceived effectiveness in achieving specific anatomy learning outcomes (LOs). Methods A cross-sectional online survey was administered to a total of 317 (Year 1–5) medical students at a private Malaysian medical university using convenience sampling. Participants ranked different anatomy teaching resources and rated their usefulness across 12 defined LOs. Data was analyzed using non-parametric statistical tests. Results Of 317 respondents, prosection of human tissues emerged as the most preferred and effective gross anatomy resource (53.3 %), followed by plastic anatomical models and online multimedia materials, while printed resources were least favored. For histology, light microscopy (LM) was preferred by 61 % of students, although both LM and virtual microscopy (VM) were perceived as comparably effective in meeting learning objectives. Preferences varied significantly by academic phase and country of origin but not by gender. Conclusion Medical students favored hands-on and visually rich learning modalities that provide tactile and spatial engagement. These findings highlight the continued relevance of prosection of human tissues and LM in anatomy education while supporting a blended teaching approach that integrates digital resources to complement traditional methods and optimize student engagement and learning outcomes. Keywords Anatomy education, Medical students, Teaching resources, Prosection of human tissues, Light microscopy, Blended learning
Major depressive disorder (MDD) is a multifactorial condition shaped by neurobiological, psychological, and environmental influences. Recent evidence highlights the gut–brain axis (GBA), a bidirectional communication system linking the gastrointestinal tract and central nervous system, as an important contributor to MDD pathogenesis via microbiota-mediated mechanisms. This narrative review synthesizes findings from preclinical and clinical studies published in the last decade, with emphasis on mechanistic insights from animal models and translational data from human cohorts. Key pathways include the microbial regulation of neurotransmitter production, immune modulation, vagus nerve signalling, and the metabolism of short-chain fatty acids (SCFAs). Dysbiosis in MDD is frequently characterized by reductions in butyrate-producing genera and elevations in pro-inflammatory taxa which have been linked to neuroinflammation, impaired neurotransmitter synthesis, and hypothalamic-pituitary-adrenal (HPA) axis dysregulation. Interventions such as probiotics, prebiotics, synbiotics, and psychobiotics show promise in alleviating depressive symptoms by modulating the gut microbiota. Emerging evidence also supports the beneficial roles of postbiotics, non-viable microbial products with immunomodulatory and neuroactive potential. Overall, microbial modulation offers a novel adjunctive strategy for depression management, particularly in treatment-resistant cases or to reduce the side effects of conventional drugs. However, heterogeneity in study design, small sample sizes, and limited causal evidence underscore the need for rigorous, large-scale trials. Future directions should prioritize identification of microbial biomarkers, optimization of strain-specific and dose–response data, and integration of gut-targeted approaches into personalized mental healthcare.
Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, multiple sclerosis, and amyotrophic lateral sclerosis share converging mechanisms of neuronal dysfunction, including protein aggregation, oxidative stress, and chronic neuroinflammation. Glial cells, once considered passive supporters, are now recognized as central drivers of these processes, offering both pathogenic triggers and therapeutic opportunities. Yet, despite compelling preclinical evidence, the translation of glial-targeted therapies into clinical success has been limited. This review provides a critical synthesis of current knowledge by examining therapeutic strategies through the lens of their translational challenges and failures. This narrative review highlights how interspecies variability of glial phenotypes, shifting neuroprotective versus neurotoxic states, limited biomarker stratification, and delivery barriers have constrained trials, such as anti-triggering receptor expressed on myeloid cells 2 (anti-TREM2) antibodies in AD and glial cell line-derived neurotrophic factor (GDNF) in PD. By analyzing these obstacles across major neurodegenerative disorders, this review argue that the next stage of glial medicine requires precision approaches that integrate stage-specific phenotyping, biomarker-guided patient selection, and innovative delivery platforms. Understanding not only what has been tried but why translation has stalled is essential to chart a roadmap for effective, disease-modifying glial therapies in the aging brain.
Neisseria gonorrhoeae is a Gram-negative diplococcus that causes gonorrhea through sexual contact. This ancient STD remains a major public health concern due to reproductive health impacts, antimicrobial resistance (AMR), and lack of a vaccine. Cannabis sativa contains antibacterial cannabinoids, though its role in combating antibiotic resistance is underexplored. The 2Fe-2S iron–sulfur cluster protein is a potential antibiotic target, as these clusters are vital for bacterial proteins involved in electron transport, enzyme activity, and gene regulation. Disrupting them may impair bacterial survival and function. In this investigation, the 2Fe–2S iron sulfur cluster binding domain-containing protein (NGFG_RS03485), identified as a potential therapeutic target from the core proteome of 12 Neisseria gonorrhoeae strains, was selected for this study. Potential antimicrobial agents were explored through molecular docking studies involving 16 cannabinoid analogs—9 obtained from literature sources and 7 identified via fingerprint similarity searches. The study revealed that four cannabinoids form favorable bonds with active regions against our targeted protein; with a high binding affinity formed from the molecular docking; 1,3-Benzenediol, 2-[3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-, (1R-trans). Dronabinol, Cannabinolic acid A (CBNA), Cannabigerolic acid (CBGA), and Ferruginene C are derivatives identified. Drug-likeness assessments were conducted to evaluate the pharmacokinetic and toxicity properties of the cannabinoids and compared against the antibiotics. Keywords: molecular docking; Cannabis sativa L.; antibiotic; cannabinolic acid; iron sulfur cluster
Background/Objectives: Cerebral small vessel disease (CSVD) often manifests as enlarged perivascular spaces (ePVS), which are linked to reduced processing speed even in asymptomatic individuals. Glymphatic dysfunction (or glymphopathy) has been proposed as a mechanism underlying ePVS, with the diffusion tensor image analysis along the perivascular space (DTI-ALPS) index serving as a potential non-invasive surrogate marker. This study aimed to examine the association between DTI-ALPS index, ePVS burden, and processing speed in community-dwelling adults without overt neurological symptoms, stratified by QRISK3 cardio-cerebrovascular risk prediction score. Methods: Sixty young-to-middle-aged adults (aged 25–65 years), classified as low-to-moderate QRISK3 scores, underwent brain 3T diffusion magnetic resonance imaging (MRI) to evaluate ePVS burden and calculate DTI-ALPS indices. Processing speed index (PSI) was assessed using the Wechsler Adult Intelligence Scale—Version IV (WAIS-IV). Results: Approximately 43% of subjects reported having ePVS with significantly lower DTI-ALPS indices and PSI compared to those without ePVS. The DTI-ALPS index was inversely correlated with ePVS burden and positively correlated with PSI. Mediation analysis showed that the lower DTI-ALPS partially mediated the association between ePVS burden and slower processing speed. Conclusions: Visible ePVS in our cohort may reflect early glymphopathy and subtle cognitive slowing, while the DTI-ALPS index may serve as an early biomarker for preclinical CSVD-related cognitive vulnerability, supporting targeted prevention strategies. Keywords: cerebral small vessel disease; enlarged perivascular spaces; glymphatic system; processing speed; diffusion tensor imaging
Background Silent cerebral small vessel disease (CSVD), marked by white matter hyperintensities (WMHs), are commonly detected incidentally on neuroimaging. Emerging evidence links early brain microstructural changes to modifiable cardio-cerebrovascular risks, even without neurological symptoms. This study aimed to explore the relationship between cardio-cerebrovascular risk, white matter tract integrity, and cognitive performance in asymptomatic adults, using QRISK3 profiling, diffusion tensor imaging (DTI), and neurocognitive evaluation. Methods Sixty neurologically asymptomatic adults (mean age: 39.8 ± 11.5 years) with low to moderate QRISK3 scores underwent standardized neurocognitive assessment 3T brain MRI, including DTI sequences. Lesion-guided region-of-interest (ROI) tractography was used to assess six bilateral white matter tracts commonly affected in CSVD: the anterior and superior corona radiata and the superior longitudinal fasciculus (SLF). Results WMHs were identified in 20 individuals (33.3 %). Their presence was significantly associated with aging, systolic blood pressure, hypertension, and QRISK3 score (p < 0.05). While no significant cognitive impairment was observed, processing speed was negatively correlated with age and QRISK3. Although DTI metrics such as fractional anisotropy (FA) and mean diffusivity (MD) did not significantly differ across groups, tract-specific analysis revealed that higher QRISK3 scores were significantly associated with reduced white matter integrity in the left SLF. Conclusion These findings highlight the presence of early, subclinical white matter alterations in individuals at cardio-cerebrovascular risk, even in the absence of neurological symptoms. The integration of tract-specific DTI analysis with vascular risk profiling may provide a sensitive approach for detecting preclinical CSVD and guiding early intervention strategies in at-risk populations. Keywords Cerebral small vessel disease; White matter integrity; Diffusion tensor imaging; QRISK3; Microstructure
ntermittent fasting (IF) is emerging as a heterogeneous neurometabolic intervention with the possibility of changing the course of neurodegenerative diseases. Through the modulation of the gut–brain axis (GBA), cellular bioenergetics (or metabolic) reprogramming, and involvement in preserved stress adaptation pathways, IF influences a range of physiological mechanisms, including mitobiogenesis, autophagy, circadian rhythm alignment, and neuroinflammation. This review critically synthesises current preclinical and early clinical evidence illustrating IF’s capability to supplement synaptic plasticity and integrity, reduce toxic proteins (proteotoxic) burden, and rehabilitate glial and immune homeostasis across models of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. The key players behind these effects are bioactive metabolites such as short-chain fatty acids (SCFA) and β-hydroxybutyrate (BHB), and molecular mediators such as brain-derived neurotrophic factor (BDNF). We feature the therapeutic pertinence of IF-induced changes in gut microbiota composition, immune response, and mitochondrial dynamics, and we discuss emerging approaches for merging IF into precision medicine frameworks. Crucial challenges include individual variability, protocol optimisation, safety in cognitively vulnerable populations, and the need for biomarker-guided, ethically grounded clinical trials. Finally, we propose IF as a scalable and flexible intervention that, when personalised and integrated with other modalities, may reframe neurodegeneration from a model of irreversible decline to one of modifiable resilience. Keywords: intermittent fasting; gut–brain axis; neurodegenerative diseases; metabolic reprogramming; SCFAs; autophagy
The COVID-19 pandemic has revealed the profound and lasting impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the nervous system. Beyond acute infection, SARS-CoV-2 acts as a potent immunomodulatory agent, disrupting immune homeostasis and contributing to persistent inflammation, autoimmunity, and neurodegeneration. Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), is characterized by a spectrum of neurological symptoms, including cognitive dysfunction, fatigue, neuropathy, and mood disturbances. These are linked to immune dysregulation involving cytokine imbalance, blood–brain barrier (BBB) disruption, glial activation, and T-cell exhaustion. Key biomarkers such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NFL) correlate with disease severity and chronicity. This narrative review examines the immunopathological mechanisms underpinning the neurological sequelae of long COVID, focusing on neuroinflammation, endothelial dysfunction, and molecular mimicry. We also assess the role of viral variants in shaping neuroimmune outcomes and explore emerging diagnostic and therapeutic strategies, including biomarker-guided and immune-targeted interventions. By delineating how SARS-CoV-2 reshapes neuroimmune interactions, this review aims to support the development of precision-based diagnostics and targeted therapies for long COVID-related neurological dysfunction. Emerging approaches include immune-modulatory agents (e.g., anti-IL-6), neuroprotective drugs, and strategies for repurposing antiviral or anti-inflammatory compounds in neuro-COVID. Given the high prevalence of comorbidities, personalized therapies guided by biomarkers and patient-specific immune profiles may be essential. Advancements in vaccine technologies and targeted biologics may also hold promise for prevention and disease modification. Finally, continued interdisciplinary research is needed to clarify the complex virus–immune–brain axis in long COVID and inform effective clinical management. Keywords: COVID-19; SARS-CoV-2; neurological disease; immune system; long COVID-19
Centella asiatica (C. asiatica) has attracted significant scientific interest due to its extensive medicinal properties and long-established use in traditional medicine. This review synthesizes recent advances in the technological exploitation of C. asiatica, covering the extraction of bioactive constituents to product development. Modern extraction techniques such as supercritical fluid extraction (SFE) and microwave-assisted extraction (MAE) have substantially improved the yield, selectivity, and preservation of key phytochemicals, particularly triterpenoids, saponins, and flavonoids. These compounds are now routinely characterized using advanced analytical platforms, ensuring product quality, consistency, and standardization. Moreover, the use of innovative formulation technologies and advanced delivery systems has facilitated the development of C. asiatica-based products tailored for various therapeutic areas, including pharmaceuticals, nutraceuticals, and cosmeceuticals targeting neuroprotection, wound healing, skin aging, and stress modulation. Alongside these developments, stringent quality control protocols, toxicological evaluations, and adherence to evolving regulatory standards enhance the safety and efficacy of C. asiatica-derived interventions. This review highlights the integration of traditional knowledge with modern science across the domains of extraction, analysis, formulation, and regulation. It serves as a comprehensive resource for researchers, formulators, and regulatory stakeholders aiming to develop high-quality, evidence-based C. asiatica products with improved bioavailability and therapeutic value. Keywords: Centella asiatica; triterpenoids; analytical; quality control; extraction
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles. Recent evidence highlights autophagy as a pivotal mechanism in cellular homeostasis, mediating the clearance of misfolded proteins and damaged organelles. However, impaired autophagy contributes significantly to AD pathogenesis by disrupting proteostasis, exacerbating neuroinflammation, and promoting synaptic dysfunction. This review aims to scrutinize the intricate relationship between autophagy dysfunction and AD progression, explaining key pathways including macroautophagy, chaperone-mediated autophagy (CMA), and selective autophagy processes such as mitophagy and aggrephagy. This further extends the discussion beyond the central nervous system, evaluating the role of hepatic autophagy in Aβ clearance and systemic metabolic regulation. An understanding of autophagy’s involvement in AD pathology via various mechanisms could give rise to a novel therapeutic strategy targeting autophagic modulation to mitigate disease progression in the future. Keywords: Alzheimer’s disease; autophagy; amyloid-beta clearance; tau pathology; neurodegeneration
Background Sciatic nerve injury, characterised by radiating pain from the lumbosacral region and associated motor-sensory deficits, remains a challenging condition with limited regenerative therapies. Clitoria ternatea (CT), a medicinal plant known for its neuroprotective and anti-inflammatory properties, has shown promise in promoting nerve regeneration. This study aimed to evaluate the therapeutic efficacy and safety of CT extract in a rat model of sciatic nerve crush injury. Methodology A total of 54 Sprague-Dawley rats were divided into six groups: normal, toxicity control, negative control (injury without treatment), positive control (methylcobalamin), and three CT treatment groups (250, 500, and 1000 mg/kg/day for 28 days). Results Hepatic and renal histology confirmed no toxicity in CT-treated groups. Functional recovery was assessed on days 14 and 28 using walking track analysis, rotarod, toe-spreading reflex, and hot plate tests, all showing significant improvement in CT-treated and positive control groups. Muscle histology (gastrocnemius, soleus, and extensor digitorum longus) and weight analysis revealed reduced atrophy and enhanced regeneration, particularly in the high-dose CT and positive groups. Morphometric evaluation using toluidine blue and cresyl violet staining indicated accelerated remyelination and increased neuronal cell body preservation. Transmission electron microscopy (TEM) further demonstrated increased myelin sheath thickness in treated groups. Conclusion These findings suggest that CT promotes axonal regrowth and functional recovery without detectable toxicity. This study provides novel preclinical evidence supporting the neuro regenerative and protective potential of Clitoria ternatea in peripheral nerve injuries, highlighting its promise as a plant-based therapeutic candidate for future translational applications. Keywords Sciatic nerve injury; Clitoria ternatea; Nerve regeneration; Therapeutic potential; Peripheral nerve injuries
The neurogenic locus notch homolog protein 3 (NOTCH3), is central in both vasculogenesis and oncogenesis and, therefore, has been considered an important factor in the development of cerebral small vessel disease (CSVD) and breast cancer (BC). Pathogenic mutations of NOTCH3 induce vascular smooth muscle cell degeneration, microvascular dysfunction and neurovascular damage in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is a genetic cause of CSVD. Meanwhile, NOTCH3 aberrant signalling in BC promotes tumour progression, metastasis and chemoresistance, especially in aggressive subtypes, such as triple-negative BC. A growing body of evidence points to a common molecular pathway whereby NOTCH3 dysregulation mediates vascular and tumour pathologies, thus providing an important link between these conditions. This narrative review synthesises current insights into the dual role of NOTCH3, focusing on translational relevance as a therapeutic target. Targeting NOTCH3 may mitigate vascular damage in CSVD and simultaneously inhibit tumour progression and metastasis in BC. The review further discusses NOTCH3 as a biomarker for early diagnosis and risk stratification, besides novel therapeutic strategies involving γ-secretase inhibitors and monoclonal antibodies. Future directions include studies into the ligand-independent functions of NOTCH3, its role within the tumour microenvironment, and the development of therapies with dual-action potential. This review discusses, for the 1st time, common mechanisms between CSVD and BC, thereby opening new avenues for therapies that could effectively target both conditions. By translating these laboratory findings into clinical applications, this approach aims to improve outcomes for patients affected by these devastating disorders.
The glymphatic system, a vital brain perivascular network for waste clearance, hinges on the functionality of the aquaporin 4 (AQP4) water channel. Alarmingly, AQP4 single nucleotide polymorphisms (SNPs) are linked to impaired glymphatic clearance, or glymphopathy, which contributes to sleep disturbances and various age-related neurodegenerative diseases. Despite the critical role of glymphopathy and sleep disturbances in cerebral small vessel disease (CSVD) – a silent precursor to age-related neurodegenerative disorders – their interplay remains underexplored. CSVD is a major cause of stroke and dementia, yet its pathogenesis is not fully understood. Emerging evidence implicates glymphopathy and sleep disorders as pivotal factors in age-related CSVD, exacerbating the condition by hindering waste removal and compromising blood-brain barrier (BBB) integrity. Advanced imaging techniques promise to enhance diagnosis and monitoring, while lifestyle modifications and personalised medicine present promising treatment avenues. This narrative review underscores the need for a multidisciplinary approach to understanding glymphopathy and sleep disorders in CSVD. By exploring their roles, emphasising the necessity for longitudinal studies, and discussing potential therapeutic interventions, this paper aims to pave the way for new research and therapeutic directions in CSVD management. Keywords: Cerebral small vessel disease, glymphatic system, sleep, aquaporin 4, glymphopathy
Introduction The extensor digitorum communis (EDC) is essential in finger extension. Its tendons vary in distribution among and between different populations. These variations in anatomy can be very important for the diagnosis and management of hand injuries among hand surgeons, anatomists, and clinicians. This study is done to assess the variation of EDC tendons among the Burmese population and assess their distribution patterns on both hands. Methods This is a cross-sectional anatomical study involving 32 cadavers (16 formalin-preserved and 16 fresh-frozen-acquired) from various medical institutions in Myanmar. A total of 64 dissected hands were observed for the number, pattern, and distribution of EDC tendons to the index (IF), middle (MF), ring (RF), and little fingers (LF). The Chi-square test was used to determine the statistical significance of tendon variations among the hands. Results All IF had a single EDC tendon (100 %). The MF had single (50 %), double (37.5 %), and triple (10.9 %) tendons. The ring finger displayed single (9.4 %), double (50 %), triple (35.9 %), and quadruple (4.7 %) tendons. The LF showed an absent EDC tendon (60.9 %), a single tendon (34.4 %), and a double tendon (4.7 %). Asymmetrical tendon distribution was observed in 62 % of cadavers. Statistical analysis confirmed significant variations in EDC tendon distribution (p < 0.001). Conclusion This study represents valuable data on anatomical variations in EDC tendons among a Burmese population and emphasises an individualised approach to surgery when dealing with tendon repair or hand reconstruction. The high incidence of asymmetrical patterns may alter functional and biomechanical results. Further investigation with advanced imaging techniques and samples of larger sizes is recommended regarding clinical implications.
Epilepsy is the second most common neurological disorder and affects approximately 50 million people worldwide. Despite advances in antiepileptic therapy, about 30% of patients develop refractory epilepsy. Recent studies have shown sleep, glymphatic function, cerebral small vessel disease (CSVD), and epilepsy are interrelated by sharing a multidirectional relationship in influencing their severity and progression. Sleep plays a vital role in brain homeostasis and promotes glymphatic clearance responsible for the removal of metabolic wastes and neurotoxic substances from the brain. Disrupted sleep is a common feature in epilepsy and can lead to impairment in glymphatic efficiency or glymphopathy, promoting neuroinflammation and accrual of epileptogenic factors. CSVD, occurring in up to 60% of the aging population, further exacerbates neurovascular compromise and neurodegeneration by increasing seizure susceptibility and worsening epilepsy outcomes. This narrative review aims to discuss the molecular and pathophysiological inter-relationships between these factors, providing a new framework that places glymphopathy and CSVD as contributors to epileptogenesis in conditions of sleep disruption. We propose an integrative model wherein the glymphopathy and vascular insufficiency interact in a positive feedback loop of sleep disruption and increased seizure vulnerability mediated by epileptic activity. Acknowledging these interactions has significant impacts on both research and clinical practice. Targeting sleep modulation, glymphatic function, and cerebrovascular health presents a promising avenue for therapeutic intervention. Future research should focus on developing precision medicine approaches that integrate neuro-glial-vascular mechanisms to optimize epilepsy management. Clinically, addressing sleep disturbances and CSVD in epilepsy patients may improve treatment effectiveness, reduce seizure burden, and improve overall neurological outcomes. This framework highlights the need for interdisciplinary approaches to break the vicious cycle of epilepsy, sleep disturbance, and cerebrovascular pathology, paving the way for innovative treatment paradigms.
Background Neuron-glial 2 (NG2) cells, or polydendrocytes, are dynamic glial cells in the central nervous system (CNS) that contribute to neuroinflammation and neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. These cells interact with neurons, astrocytes, and microglia, modulating inflammatory responses, synaptic activity, and blood-brain barrier integrity. While NG2 cells have protective roles, their aberrant activation can contribute to scarring, inflammation, and neuronal degeneration. Methods This narrative review synthesizes current literature on the molecular and functional properties of NG2 cells with a focus on their involvement in neuroinflammation and neurodegeneration. Relevant studies were identified through searches in PubMed, Scopus, and Google Scholar, using keywords such as “NG2 cells,” “neuroinflammation,” and “neurodegenerative diseases.” Articles were selected based on relevance to NG2 cell biology, their interactions with other glial cells, and their therapeutic implications. Findings were categorized into key themes, including NG2 cell activation, inflammatory signaling, and potential therapeutic targets. Conclusion NG2 cells are key players in neuroinflammation and neurodegeneration, serving both protective and pathological roles. Understanding their mechanisms of action can aid in identifying therapeutic strategies targeting NG2 cell activation, including anti-inflammatory agents, epigenetic modulators, natural compounds, and monoclonal antibodies. Future research should explore NG2 cell-targeted interventions to develop novel treatments for CNS disorders.
Background: Surfactant protein-A (SP-A) is the most prevalent protein in the pulmonary surfactant system and it is expressed in Type II alveolar epithelial cells. Materials and methods: We evaluated SP-A expression in 92 fetal human lungs at various gestational ages in Myanmar (Burma) using hematoxylin and eosin staining and immunohistochemical assays. Results: We detected tubular structures in the fetal lungs during the canalicular stage of development at gestational weeks 22–25. Bronchioles were detected between 26–27 and 28–33 weeks, when primitive alveoli were evident. At 34–40 weeks, clusters of alveolar sacs opened from the alveolar ducts during the saccular development stage. At 40–44 weeks, extremely thin alveolar walls resembled sections of adult lungs. Type II cells secreting surfactant were undetectable at 22–25 weeks, but became detectable from 26 weeks, and the abundance of Type II cells increased after 28 weeks. Surfactant spread throughout the alveoli at 34 weeks. Because the positivity index of these cells significantly correlated with a gestational age of 26–33 weeks, we established a formula to estimate gestational age. Conclusions: Our findings improve understanding of fetal lung development and maturity, and provide valuable insights into the diagnosis and management of respiratory disorders among premature infants in Myanmar. Keywords: surfactant protein-A; human fetal lung; histology; immunohistochemistry; Myanmar
The human microbiota constitute a very complex ecosystem of microorganisms inhabiting both the inside and outside of our bodies, in which health maintenance and disease modification are the main regulatory features. The recent explosion of microbiome research has begun to detail its important role in neurological health, particularly concerning cerebral small vessel disease (CSVD), a disorder associated with cognitive decline and vascular dementia. This narrative review represents state-of-the-art knowledge of the intimate, complex interplay between microbiota and brain health through the gut–brain axis (GBA) and the emerging role of glymphatic system dysfunction (glymphopathy) and circulating cell-derived microparticles (MPs) as mediators of these interactions. We discuss how microbial dysbiosis promotes neuroinflammation, vascular dysfunction, and impaired waste clearance in the brain, which are critical factors in the pathogenesis of CSVD. Further, we discuss lifestyle factors that shape the composition and functionality of the microbiota, focusing on sleep as a modifiable risk factor in neurological disorders. This narrative review presents recent microbiome research from a neuroscientific and vascular perspective to establish future therapeutic avenues in targeting the microbiota to improve brain health and reduce the burden of CSVD.
Neuron-Glial2 (NG2) expressing cells are described as the oligodendrocyte precursor cells in the brain. This study aimed to investigate the possible involvement of NG2 cells under the methamphetamine (METH)-induced neurotoxicity and neuroprotective capacity of melatonin. The results showed that the levels of NG2 in rat brain gradually increase from postnatal day 0 to postnatal day 8 and then the lower levels of NG2 are shown in adults. In adult rats, the levels of NG2 and COX-2 in the brain were significantly increased in lipopolysaccharide treatment. Pretreatment of 10 mg/kg melatonin prior to treating with METH was able to reduce an increase in the levels of NG2 and activation in astrocyte and microglia. These findings would extend the contribution of NG2 expressing cells in the adult brain during pathological conditions such as neuroinflammation.