Delirium-associated sleep disorder is often linked to circadian rhythm dysregulation, in which the melatonin 1 (MT1) receptor plays a central role. The purpose of this study was to investigate the agonistic potential of Avena sativa derived phytocompounds against the MT1 receptor and to identify promising natural candidates for managing delirium-related sleep disturbances using in silico approaches. Phytocompounds derived from A. sativa were initially screened using the IMMPAT 2.0 server. Selected compounds, namely luteolin, apigenin, tricin, isovitexin, and vitexin, were docked against the MT1 receptor using PyRx 0.8. Pharmacokinetic and toxicity profiling were performed using Deep-PK and ProTox-III to assess ADME/T properties. Drug-likeness was evaluated based on Lipinski’s rule of five, and blood–brain barrier permeability was assessed using the MolSoft server. Molecular interactions were visualised and analysed using Discovery Studio. Molecular dynamics (MD) simulations were conducted to evaluate the stability of ligand-MT1 receptor complexes in comparison with the reference drug ramelteon. All five phytocompounds exhibited favourable docking scores ranging from − 7.9 to − 9.6 kcal/mol. Tricin showed unfavourable drug-likeness properties, while isovitexin and vitexin failed to meet acceptable toxicity criteria. Apigenin and luteolin demonstrated strong binding affinity, favourable pharmacokinetic profiles, acceptable toxicity and stable interactions with key MT1 receptor residues. MD simulation results revealed that both apigenin and luteolin formed stable complexes with the MT1 receptor, which were comparable to ramelteon. Luteolin exhibited slightly enhanced compactness, while apigenin showed stability closely resembling the standard ligand. The findings suggest that apigenin and luteolin are promising modulators of the MT1 receptor with potential therapeutic relevance for delirium-associated sleep disorders. However, further in vitro and in vivo studies are required to validate their efficacy and safety.

Chronic stress is a major public health concern, contributing to a spectrum of physiological and psychological disorders, including anxiety, depression, cardiovascular diseases, and metabolic syndromes. This review examines the epigenetic mechanisms mediating the impact of chronic stress on human health, focusing on DNA methylation, histone modifications, and non-coding RNAs. These epigenetic alterations act as dynamic interfaces between environmental stressors and genomic responses, modifying gene expression in critical stress-related pathways, such as the hypothalamic-pituitary-adrenal (HPA) axis and neurotrophic factors like BDNF. The significance of this research lies in elucidating how these epigenetic changes, induced by early-life adversity, socioeconomic pressures, and environmental toxins, create lasting molecular imprints that increase susceptibility to stress-related disorders and can be transmitted across generations. Key findings include stress-induced hypermethylation of the glucocorticoid receptor gene (NR3C1), histone acetylation changes in brain regions like the hippocampus and amygdala, and the regulatory roles of microRNAs (e.g., miR-132) and long non-coding RNAs (e.g., HOTAIR). These modifications disrupt neural plasticity, emotional regulation, and cognitive function, while also contributing to physical health outcomes, including inflammation, metabolic dysregulation, and cancer. The review also explores therapeutic interventions, such as DNA methylation inhibitors (e.g., 5-azacytidine), histone deacetylase inhibitors (HDACIs), and lifestyle modifications like mindfulness and dietary polyphenols. By integrating molecular insights with clinical perspectives, this article underscores the critical role of epigenetic research in developing targeted interventions to mitigate the enduring effects of chronic stress, offering transformative potential for personalized medicine and public health strategies.

The current study aimed to explore the anxiolytic effects of phytochemicals present in Nigella sativa (black cumin) plant seeds. For that purpose, first we identified a plethora of bioactive phytocompounds by performing gas chromatography and mass spectrometry (GC–MS) analysis. GC–MS results revealed a total of 38 phytochemicals, including Guanosine 29.80

Irritable Bowel Syndrome (IBS) is a prevalent functional gastrointestinal disorder characterized by abdominal pain, bloating, and altered bowel habits in the absence of detectable structural or biochemical abnormalities. Despite its high global burden, the pathophysiology of IBS remains largely unknown. Current evidence suggests that IBS arises from multifactorial interactions involving genetic predisposition, visceral hypersensitivity, gut microbiota dysbiosis, immune dysregulation, and disturbances in the gut–brain axis. Psychosocial factors such as stress, anxiety, and depression further contribute to symptom severity. This review aims to summarize the current understanding of IBS pathogenesis and discuss emerging integrative management strategies. A narrative review of recent literature was conducted, focusing on advances in IBS pathophysiology, diagnostic criteria, and therapeutic approaches. Studies related to microbiome alterations, immune and serotonergic signalling, and novel pharmacological and non-pharmacological treatments were examined. Diagnostic classification based on the Rome IV Criteria for Functional Gastrointestinal Disorders was also considered. IBS is classified into four clinical subtypes according to predominant bowel patterns: IBS with diarrhea (IBS-D), IBS with constipation (IBS-C), mixed IBS (IBS-M), and unclassified IBS (IBS-U). Increasing evidence highlights the roles of microbiome imbalance, immune activation, altered serotonergic pathways, and genetic susceptibility in disease progression. Recent therapeutic developments include targeted pharmacological agents such as Eluxadoline, Lubiprostone, and Rifaximin, alongside adjunctive treatments including selective serotonin reuptake inhibitors and probiotics. Dietary modification (e.g., low-FODMAP diet, increased soluble fiber), physiotherapy, and psychological interventions such as cognitive behavioral therapy and gut-directed hypnotherapy also demonstrate significant clinical benefit. IBS management requires a comprehensive, multidisciplinary approach integrating pharmacological, dietary, and psychological interventions. Future research focusing on personalized and microbiome-targeted therapies may further improve outcomes and quality of life in IBS patients.

Objective: To investigate the chronotherapeutic potential of phytochemicals from Withania somnifera (ashwagandha) leaf extract as histamine H3 receptor (H3R) inhibitors for suppressing H3R overexpression to manage excessive daytime sleepiness (EDS) and muscle weakness (cataplexy) in narcolepsy.Methods: Gas chromatography–mass spectrometry (GC-MS) was used to identify 43 phytoconstituents in W. somnifera leaf extract. Molecular docking was performed to evaluate H3R-binding affinity of these compounds. Physicochemical properties, drug-likeness, blood-brain barrier permeability, and the absorption, distribution, metabolism, excretion, and toxicity (ADMET) analysis were done to evaluate drug-like characteristics. Molecular dynamics simulations and molecular mechanics/generalized Born surface area (MM/GBSA) calculations were conducted to validate binding stability, and protein-ligand interactions were visualized to identify key binding mechanisms.Results: GC-MS analysis identified major compounds, including 2-methoxy-4-vinylphenol and hexadecanoic acid. Molecular docking revealed methotrexate, 1,2-benzenedicarboxylic acid, octadecenoic acid, adenosine 3',5'-cyclic monophosphate, and 9,12-octadecadienoyl chloride as top H3R-binding candidates with docking scores ranging from -8.8 to -6.2 kcal/mol. Methotrexate and adenosine 3',5'-cyclic monophosphate exhibited favorable stability and safety profiles in ADMET analyses. Molecular dynamics and MM/GBSA confirmed stable binding, with key hydrogen bonds and hydrophobic interactions observed with H3R residues.Conclusion: Phytochemicals from W. somnifera, particularly methotrexate, 1,2-benzenedicarboxylic acid, and adenosine 3',5'-cyclic monophosphate, show promise as novel plant-based H3R inhibitors for managing EDS and cataplexy in narcolepsy. These findings support their potential as safer alternatives to current treatments; nevertheless, further in vivo clinical validation is needed.

The current study aimed to conduct a phytochemical screening of commonly known Withania somnifera leaf extract through gas chromatography and mass spectrometry (GC–MS) to identify the bioactive compounds responsible for its MAO-A inhibitory action and evaluate the pharmacological potentialities of the extract and its fractions against anxiety. In the in-silico analysis, various tools were employed, including molecular docking and molecular dynamics (MD) simulation. These methods assessed the binding affinity and stability of the phytochemicals (ligands) with MAO-A. The preclinical efficacy and safety of the phytochemicals were evaluated using ADMET/T analysis. Furthermore, the biological activity of the selected phytochemicals as potential “MAO-A” inhibitors was assessed using PASS analysis. Lipinski’s rule of five was applied to predict the drug-likeness properties of the compounds. The interacting residues and the types of interactions between the active site of MAO-A and the compounds were evaluated. The cumulative results of these analyses identified 2-Methoxy-4-vinylphenol, Hexadecanoic acid, N,N-Bis(2-hydroxyethyl) dodecanamide, 1,2 Benzene dicarboxylic acid diethyl ester, and Oxacycloheptadec-8-en-2-one as hit compounds from W. somnifera, suggesting their potential as MAO-A inhibitors. This research aims to provide an elaborative description of promising phytochemical entities with activities against MAO-A. However, the efficacy of these phytochemicals as potential anxiolytic compounds needs further validation via in vitro and in vivo studies.

The neuropeptide orexin/hypocretin plays a crucial role in numerous physiological processes such as regulation of sleep/wakefulness, appetite and emotions. Dysregulation of orexin signaling has been implicated in hypersomnia, especially in narcolepsy, characterized by excessive daytime sleepiness (EDS), sudden loss of muscle tone while awake (cataplexy), sleep paralysis, and hallucinations. Lack of orexins contributes to the development of narcolepsy, thus small-molecule orexin receptor agonists are promising therapeutics for narcolepsy. In this study, we employed several bioinformatics tools to screen and identify effective phytochemicals of Rauvolfia serpentina that may act as Orexin 2 receptor (OX2R) agonists. In silico methods such as protein‒ligand interaction analysis, drug‒likeness evaluation, ADMET analysis, molecular docking, molecular dynamics simulation, and biological activity prediction, have been employed extensively. Among all screened phytochemicals from R. serpentina, both tetraphylline and yohimbine were identified as promising drug candidates due to their favorable ADMET profile, high docking scores, permeability of the blood‒brain barrier, and significant RMSD, RMSF, Rg, and SASA values. However, the study is solely based on in silico study, therefore in vitro and in vivo experimental studies are suggested to validate the potency and efficacy of these medications.

This study examines the impact of social media (SM) usage on sleep quality and its consequences for the mental and physical well-being of graduate research scholars in India. In a cross-sectional study of 119 randomly selected participants aged 24–29 years, physiological (heart rate, SpO2, blood pressure) and psychological (depression-D, anxiety-A, stress-S) parameters were measured using the DASS-21 inventory. Statistical analyses were conducted using IBM SPSS Statistics 25 and Jupyter Notebook, revealing that increased SM usage before bedtime significantly disrupts sleep patterns, exacerbating depression, anxiety, and stress. Comparative analyses of gender differences showed females experienced a higher prevalence of sleep disruptions and psychological ailments than males. Statistical analysis of the raw data revealed a positive correlation among variables D, A, and S. When the correlations between psychometric scale parameters and physiological parameters were examined, notable trends emerged. Specifically, D exhibited a negative correlation (r = -0.33) with SpO2, with a p-value of 0.000155. This negative correlation suggested that SpO2 levels tend to decrease in individuals experiencing depression, possibly due to symptoms such as shortness of breath. Additionally, the correlation coefficient between D and BPM was reported to be 0.28, with a p-value of 0.000155. Similarly, A was negatively correlated (r= -0.27) with SpO2, with a p-value of 0.003. The correlation between A and BPM was notably stronger, with an r of 0.37 and a p-value of 0.000028. Furthermore, A exhibited a significant correlation (p-value = 0.031) with systolic BP. S demonstrated a strong positive correlation with BPM (r = 0.520, p-value = 1.0596E-9) and exhibited significant correlations with diastolic and systolic BP (p-values of 0.002466 and 2.951E-7, respectively). These findings call for urgent interventions to promote healthy SM use and sleep hygiene among scholars, particularly females, to mitigate psychological and physiological distress in high-stress academic settings.

Cancer has become a global health issue that demands transformative and advanced therapeutic approaches. Recent advancements in cancer research and therapeutics have shown that gold nanoparticles (AuNPs) possess potential anticancer, apoptotic, phagocytic, and immune modulation properties. Their unique physicochemical properties at the nanoscale make AuNPs effective candidate in various cancer therapeutics. This review uniquely highlights recent insights into the molecular mechanisms of AuNP-induced cancer cell death, cell cycle arrest, and immune modulation with multidimensional approach, an area often overlooked in earlier reviews. Also, it examines recent studies, exploring how AuNPs trigger their cancer-fighting properties such as cell death initiation, DNA destruction, and immune system modulation. AuNPs initiate cell death by targeting mitochondrial enzymes along with producing reactive oxygen species (ROS) and activating caspase proteins. AuNPs harm DNA, leading to cell cycle arrest, which in turn trigger apoptosis (programmed cell death) or other forms of cell death. Research study claims that AuNPs activate macrophages and regulate cytokine release which helps suppress tumor growth and metastasis. Moreover, this review compares chemical and green synthesis approaches, emphasizing green synthesis for its enhanced biocompatibility and alignment with targeted cancer therapy. Green synthesis methods are not only devoid of toxic chemicals but also superior in controlling particle size, shape, and surface functionality. Consequently, these green-synthesized AuNPs have been utilized in cancer research with improved therapeutic efficacy and enhanced cancer-targeting capabilities.

Major depressive disorder (MDD) affects over 280 million people globally, presenting a significant public health challenge. This review evaluates the use of citalopram, a selective serotonin reuptake inhibitor (SSRI), in MDD management, focusing on its therapeutic efficacy and the critical adverse effect of citalopram-induced hyponatremia (CIH). Through a comprehensive literature analysis, we explore the medicinal chemistry of citalopram, its mode of action, and the mechanisms underlying CIH, primarily associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Findings indicate that CIH affects 9-40% of patients, with a higher prevalence in vulnerable populations such as the elderly and cancer patients, where it complicates treatment due to interactions with disease-related factors. Routine serum sodium monitoring is recommended for individuals at risk to mitigate potential risks. The review highlights the need for tailored treatment strategies to balance citalopram’s benefits against CIH risks, particularly in cancer patients, and identifies future research directions for personalized MDD management.

Glioblastoma (GBM) is a highly aggressive brain cancer with limited therapeutic options. The epidermal growth factor receptor (EGFR) plays a critical role in tumor progression, making it a promising target for novel treatments. This study aimed to identify plant-derived phytochemicals as potential EGFR inhibitors to enhance the management of GBM. Computational approaches were utilized, including virtual screening of phytochemicals from the NPACT database against the EGFR crystal structure (PDB ID: 5XWD). Molecular docking, ADMET (absorption, distribution, metabolism, excretion, and toxicity) profiling, and 50 ns molecular dynamics (MD) simulations were performed to evaluate binding affinity, pharmacokinetic properties, and complex stability using metrics, such as root mean square deviation (RMSD), radius of gyration (Rg), and solvent-accessible surface area (SASA). Cytotoxicity was assessed against the SF-295 GBM cell line. Three phytochemicals, 2,3-dihydrowithaferin A, strophanthidin, and 6,8-diprenyleriodictyol, demonstrated strong EGFR binding affinities (-8.5 to -7.9 kcal/mol), favorable drug-like properties, and optimal ADMET profiles. MD simulations confirmed stable binding for 2,3-dihydrowithaferin A and 6,8-diprenyleriodictyol, with low RMSD (<2.5 Å), compact Rg (<2.2 nm), and reduced SASA. Only 6,8-diprenyleriodictyol exhibited cytotoxicity against SF-295 GBM cells (Pa = 0.383). The findings position 6,8-diprenyleriodictyol as a promising EGFR inhibitor due to its balanced binding affinity, pharmacokinetic profile, and selective cytotoxicity, potentially addressing limitations of current EGFR inhibitors like erlotinib in GBM. The stable binding and favorable ADMET properties suggest potential for CNS penetration; however, the P-glycoprotein substrate status warrants further investigation. However, there is a need for in vitro and in vivo validation to confirm its efficacy and selectivity. 6,8-Diprenyleriodictyol emerges as a lead candidate for EGFR-targeted GBM therapy, supported by its strong binding, favorable pharmacokinetics, and cytotoxicity against GBM cells. Further experimental studies are needed to validate its therapeutic potential and overcome challenges, such as BBB penetration.

Diabetic retinopathy (DR) is a serious sight-threatening complication that occurs due to constant hyperglycemia. It is the most common and leading cause of vision impairment worldwide. The development and progression of DR involve a complex network of genetic and environmental factors. Vascular inflammatory pathways, oxidative stress and epigenetic modifications have been linked to the development of diabetic mediated retinopathy. Candidate gene studies have implicated variants in genes involved in glucose metabolism such as (ALR2), vascular regulation (VEGF) are closely associated with DR susceptibility. Hyperglycemia triggers several factors such as polyol pathway, advanced glycation end-products (AGEs) formation, activation of protein kinase C (PKC), dysregulation of the renin-angiotensin system (RAS). These pathways collectively induce oxidative stress, inflammation, vascular dysfunction and pathological angiogenesis that further intensify microvascular lesions resulting in DR pathogenesis. Emerging therapeutic strategies present anti-VEGF agents, PKC inhibitors, and drugs modulating RAS system. In addition, targeted medicine based on genetic risk profiling and novel gene therapy approaches hold great promise in DR treatment. Further research integrating multi-omics data, gene-environment interactions, and precise translational studies are required for improving DR management and associated risk factor.

Introduction: To identify and evaluate phytochemicals from Syzygium cumini (Indian blackberry) as potential natural Dipeptidyl Peptidase-4 (DPP-4) inhibitors for the management of Type 2 Diabetes Mellitus (T2DM), aiming to find safer alternatives to synthetic inhibitors that are often associated with severe side effects. Methods: We employed different in-silico approaches to screen the phytochemicals of S. cumini for their DPP-4 inhibitory potential. Firstly, Molecular docking was performed to evaluate binding affinities with DPP-4. Subsequently, a PASS (Prediction of Activity Spectra for Substances) analysis was performed to confirm the antidiabetic potential. Furthermore, ADMET (Absorption, Distribution, Metabolism, Excretion, and Toxicity) profiling was conducted to assess pharmacokinetic properties. Lastly, Molecular dynamics (MD) simulations lasting 50 nanoseconds were performed to analyze the structural stability of protein-ligand complexes. Results: Three phytochemicals, namely astragalin, bergenin, and maslinic acid, demonstrated strong binding affinities, with docking scores of -8.4, -7.2, and -8.8, respectively. Bergenin exhibited the highest structural compactness in MD simulations, as indicated by the radius of gyration. ADMET analysis suggested all three compounds exhibited favourable pharmacokinetic and safety profiles. Discussion: The present study provides valuable insights into the potential of S. cumini phytochemicals as natural DPP-4 inhibitors. While further in-vitro and in-vivo validation is recommended, the findings offer a promising foundation for the development of safe, plant-derived therapeutics that could complement existing antidiabetic strategies. Conclusion: Phytochemicals from S. cumini, particularly astragalin, bergenin, and maslinic acid, show promise as natural DPP-4 inhibitors with potential application in T2DM treatment. These compounds offer a safer alternative to synthetic drugs.

Alzheimer’s disease (AD) is characterized by amyloid-β (Aβ) plaque accumulation, neurofibrillary tangles, neuroinflammation, and progressive cognitive decline, posing a significant global health challenge. Growing evidence suggests that dietary polyphenols may reduce the risk and progression of AD through multifaceted neuroprotective mechanisms. Polyphenols regulate amyloid proteostasis by inhibiting β/γ-secretase activity, preventing Aβ aggregation, and enhancing clearance pathways. Their strong antioxidant properties neutralize reactive oxygen species, chelate redox-active metals, and activate cytoprotective enzymes via Nrf2 signaling. This review examines the potential therapeutic targets, signaling pathways, and molecular mechanisms by which dietary polyphenols exert neuroprotective effects in AD, focusing on their roles in modulating amyloid proteostasis, oxidative stress, neuroinflammation, and cerebrovascular health. Polyphenols mitigate neuroinflammation by suppressing NF-κB signaling and upregulating brain-derived neurotrophic factor, supporting neuroplasticity and neurogenesis. They also enhance cerebrovascular health by improving cerebral blood flow, maintaining blood–brain barrier integrity, and modulating angiogenesis. This review examines the molecular and cellular pathways through which polyphenols exert neuroprotective effects, focusing on their antioxidant, anti-inflammatory, and amyloid-modulating roles. We also discuss their influence on key AD pathologies, including Aβ deposition, tau hyperphosphorylation, oxidative stress, and neuroinflammation. Insights from clinical and preclinical studies highlight the potential of polyphenols in preventing or slowing AD progression. Future research should explore personalized dietary strategies that integrate genetic and lifestyle factors to optimize the neuroprotective effects of polyphenols.

Objective: This study aimed to identify potential phytochemicals from Withania somnifera (ashwagandha) that can act as gamma-aminobutyric acid A (GABA-A) receptor agonists or stimulant, and evaluate their suitability as potential insomnia treatments. Methods: Various computational approaches were employed, including virtual screening, biological activity prediction, physicochemical and drug-likeness analysis, absorption, distribution, metabolism, excretion, and toxicity (ADME/T) analysis, and molecular dynamics simulations. The Diseases Plants Eliminate (DISPEL) server was used to identify suitable plant species in context to insomnia, and the Indian Medicinal Plants, Phytochemistry And Therapeutics 2.0 (IMPPAT 2.0) database was utilized to assess the phytochemicals from W. somnifera. Virtual screening was performed using AutoDock Vina, and biological activity prediction was carried out using the Prediction of Activity Spectra for Substances (PASS) web server. The SwissADME webserver was used for physicochemical and drug-likeness analysis, while the ADME/T analysis was conducted using the ADMETlab 2.0 and ProTox 3.0 servers. Molecular dynamics simulations were performed using the WEBGRO Macromolecular Simulations server. Results: The findings revealed that hygrine, tropine, and withasomnine exhibited promising GABA-A receptor agonist activity, favorable drug-likeness properties, low toxicity, and stable receptor-ligand interactions. These phytochemicals demonstrated desirable physiochemical properties, adhering to Lipinski’s rule of five, and exhibited favorable ADME profiles. Molecular dynamics simulations showed stable interactions between the compounds and the GABA-A receptor, with minimal conformational changes and high compactness observed for hygrine and tropine. Conclusion: The phytochemicals hygrine, tropine, and withasomnine from W. somnifera emerged as potential lead compounds for the development of novel insomnia treatments targeting the GABA-A receptor. These findings warrant further investigation through experimental validation and optimization to advance their development as potential therapeutic agents for insomnia.

In 2008, the World Health Organization (WHO) stressed major depressive disorder (MDD) as the third most important cause of disease burden worldwide. Based on their projections, it is expected that by 2030, MDD will take the lead among the rest of the world’s health concerns. Brain derived neurotrophic factor 4 (BDNF4), a protein of neurotrophins family play pivotal role in maintaining neural plasticity, and its reduced level in the hippocampus and plasma have been reported in patients with MDD. Nootropic drugs serve as therapeutic interventions in mitigating MDD through diverse molecular mechanisms. Punica granatum (pomegranate) is acknowledged for its nutritional and medicinal properties, currently under medical scrutiny for its potential as a natural antidepressant. Various computational methodologies, including molecular docking, pharmacokinetics, ADME (absorption, distribution, metabolism and excretion) profile assessment, toxicological analysis, and prediction of biological activity, were employed to identify promising compounds among the phytochemicals present in Punica extract, focusing on their potential BDNF4-stimulating, nootropic, and antidepressant properties. The comprehensive examination of docking scores, interactions between proteins and ligands, pharmacological and toxicological attributes, along with the forecasting of biological activities, collectively underscores the potential attributes of M-Cymene, Flavylium, 2-(4-Methylphenyl)propan-2-ol, Thymol, and Pelletierine as prospective drug candidates targeting human BDNF4 for alleviating MDD.

Circadian rhythms are endogenous oscillations coordinating the physiological and behavioral activities with the daily light-dark cycle and are controlled by molecular mechanisms. Nicotinamide adenine dinucleotide (NAD+), a critical cofactor in redox processes and a substrate for many enzymes, is an important metabolite in circadian rhythms. NAD+ levels show strong circadian oscillations, which are caused by the rhythmic production of biosynthetic enzymes such as nicotinamide phosphoribosyl transferase. In contrast, the circadian clock system regulates the expression of NAD+ biosynthetic enzymes, resulting in a bidirectional regulatory loop. Sirtuins, a class of NAD+-dependent protein deacetylases, regulate the circadian clock by interacting with the core clock components and transcriptional regulators. Sirtuin (SIRT) 1 deacetylates and modulates the activity of key circadian transcription factors such as brain and muscle arnt-like 1 and period circadian regulator 2, while SIRT6 regulates the expression of circadian-controlled metabolic genes. This review explored the complex relationships among NAD+, sirtuins, and the circadian clock machinery, emphasizing their roles in sustaining metabolic homeostasis and coordinating cellular processes with daily environmental cycles. Moreover, circadian disruptions are strongly associated with aging, which results in the dysregulation of NAD+ homeostasis and sirtuin activity and contributes to the development of various age-related pathologies. Strategies to restore NAD+ levels or modify the sirtuin activity have emerged as promising treatment options for circadian rhythm disturbances and age-related disorders. This review also aimed to cover new horizons in this subject, such as the development of NAD+ boosters and sirtuin modulators, chrono-pharmacological methods, and the study of epigenetic mechanisms underlying sirtuin-mediated circadian regulation.

The excessive exposure of blue light, originated from electronic gadgets like smartphones, laptops, and tablets, may contribute to sleep problems. Long exposure to blue-wavelength light from these devices affects sleep by suppressing melatonin hormone and cause neurophysiologic consequences. This literature review highlights the most recent findings on the relationship between sleep disruption and blue light exposure among the high school and college student population. A variety of scientific studies have shown that blue light exposure, especially before bedtime, can create circadian disruptions and inhibit melatonin secretion in brain, which ultimately result in deteriorated sleep quality and duration. Sleep deprivation in duration and quality of sleep is reflected in negative effects on mood, learning memory, and academic performance of a student from middle school to college. In general, the accumulating evidence indicates that, to promote adolescent and young adult health, it is necessary to pay attention to the impacts of blue light exposure from modern technologies.

The human gut microbiome dysbiosis plays an important role in the pathogenesis of Parkinson’s disease (PD). The bidirectional relationship between the enteric nervous system (ENS) and central nervous system (CNS) under the mediation of the gut-brain axis control the gastrointestinal functioning. This review article discusses key mechanisms by which modifications in the composition and function of the gut microbiota (GM) influence PD progression and motor control loss. Increased intestinal permeability, chronic inflammation, oxidative stress, α-synuclein aggregation, and neurotransmitter imbalances are some key factors that govern gastrointestinal pathology and PD progression. The bacterial taxa of the gut associated with PD development are discussed with emphasis on the enteric nervous system (ENS), as well as the impact of gut bacteria on dopamine production and levodopa metabolism. The pathophysiology and course of the disease are associated with several inflammatory markers, including TNF-α, IL-1β, and IL-6. Emerging therapeutic strategies targeting the gut microbiome include probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT). The article explored how dietary changes may affect the gut microbiota (GM) and the ways that can affect Parkinson’s disease (PD), with a focus on nutrition-based, Mediterranean, and ketogenic diets. This comprehensive review synthesizes current evidence on the role of the gut microbiome in PD pathogenesis and explores its potential as a therapeutic target. Understanding these complex interactions may assist in the development of novel diagnostic tools and treatment options for this neurodegenerative disorder.