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Suicidal behavior in children and adolescents is a major global public health issue, and suicide is one of the leading causes of death in this age group. While psychosocial determinants of suicidality are well established, understanding its biological risk factors is crucial for targeted prevention and treatment. This review presents a narrative synthesis of recent literature examining current evidence on the biological mechanisms that contribute to youth suicidality. Genetic liability plays a substantial role, often interacting with environmental stressors. Key neurobiological factors include dysfunction of the serotonin system and impaired neuroplasticity, characterized by a glutamate-gamma-aminobutyric acid imbalance and reduced brain-derived neurotrophic factor. Psychosocial stress appears linked to these changes through several pathways, including dysregulation of the hypothalamic-pituitary-adrenal axis, chronic low-grade inflammation, oxidative stress, and activation of the kynurenine pathway. Neurodevelopmental conditions like autism spectrum disorders and attention deficit hyperactivity disorder, as well as sleep disturbances, may further increase risk. While therapeutic agents such as ketamine and lithium target these neurobiological systems, evidence for their anti-suicidal efficacy in youth remains limited, with only a small number of randomized controlled trials conducted in pediatric populations. Biological research offers valuable insights, but the use of varied study methods and a lack of longitudinal data complicate its translation into clinical practice. Future studies should employ integrative, developmentally informed models to elucidate causal mechanisms and inform more effective interventions. Show less

There are limited data on the dynamic changes in daily composition of movement behaviors (sleep; moderate-to-vigorous physical activity, MVPA; light physical activity, LPA; and sedentary time, SED) and their associations with body weight in postpartum women. The purpose of this study was to examine associations of reallocating time in one behavior to another with body weight, at different times in the first year postpartum. The study included 86 women who delivered a singleton infant at ≥37 weeks gestation. Physical activity and sleep were measured via actigraphy in early, mid-, and late postpartum. Body weight was measured at each timepoint. Isotemporal substitution models were used to examine the association of reallocating ten minutes of one behavior (MVPA, LPA, SED, or sleep) to another, with body weight. Participants spent most of their day in SED (~52-53%), followed by sleep (~30%), LPA (~12-13%), and then MVPA (~2%) throughout the first year postpartum. In early and mid-postpartum, but not late postpartum, reallocating 10 min of MVPA to LPA, SED, or sleep was associated with lower body weight (range: 3.07-4.03 kg lower). In early and late postpartum, reallocating 10 min of SED to LPA was associated with a lower body weight (4.03 kg and 1.04 kg, respectively). In participants who slept ≥7 h per day, reallocating sleep to LPA in early postpartum, and MVPA time to LPA in mid-postpartum was associated with lower body weight. In those who slept <7 h, no significant associations with body weight were found when reallocating time from one behavior to another. Encouraging LPA throughout the postpartum period may be beneficial for weight loss, and having enough sleep may be especially important for early to mid-postpartum. Future research examining the impact of changes in LPA on body weight in the postpartum period are needed, along with postpartum specific 24 h movement guidelines. Show less

Rhubarb, traditionally used in China for neurological disorders, has recently attracted considerable scientific attention for its neuroprotective and cerebrovascular benefits. The main therapeutic components of rhubarb are anthraquinones, including emodin, aloe-emodin, chrysophanol, rhein, and physcion. Accumulating experimental evidence indicates that anthraquinones are of importance in neurodegenerative diseases (NDDs), such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. However, as a promising candidate for drug development, the mechanisms by which anthraquinones treat NDDs have not been systematically reviewed. Therefore, this article outlines the anti-neurodegenerative effects of anthraquinones, focusing on their molecular mechanisms. This article reviews recent research progress of anthraquinones in NDDs, focusing on their potential targets and pathways to provide new ideas for the intervention and treatment of NDDs. A comprehensive search of PubMed, Web of Science, and Google Scholar was conducted for articles on the intervention of anthraquinones in NDDs in the past 20 years. The collected information was then summarized and analyzed. Anthraquinones ameliorate NDDs through multiple mechanisms. They exhibit antioxidant and anti-inflammatory effects, protect mitochondria, and regulate microglial polarization. Furthermore, anthraquinones inhibit pyroptosis, apoptosis, tau phosphorylation, Aβ/α-synuclein aggregation, and acetylcholinesterase activity, while restoring metal homeostasis, activating estrogen receptors, modulating gut microbiota, increasing BDNF levels, and preserving blood-brain barrier permeability. More notably, these compounds play a neuroprotective role by mediating multiple signaling pathways and targets, including Nrf2, ERK1/2, PI3K/mTOR, ROS/TXNIP, SIRT1/PCG-1α, NLRP3, PI3K/Akt, MAPK, TLR4-NFκB, CaM/CaMKIV, and Ca The pleiotropic actions of anthraquinones highlight their potential as therapeutic candidates for NDDs, yet clinical validation remains essential. Future studies should emphasize rigorously designed clinical trials and optimized brain-targeted delivery platforms. This review consolidates current evidence to support their translational development. Show less

Validate the clinical utility of exosome cargo (miRNAs/proteins) and NLRP3/BDNF as key regulatory molecules for acupuncture-mediated spinal cord injury (SCI) recovery. From the establishment of the database to May 2025, a literature search was conducted on PubMed, and Embase, using keywords ["exosome cargo" or "exosome"], ["acupuncture" or "acupuncture and moxibustion" or "electroacupuncture" or "EA"], ["spinal cord injury" or "SCI"], ["immune regulation"], ["inflammatory reaction"], ["neuroregeneration" or "nerve"]. Including peer-reviewed studies on human/animal models, articles that do not meet the requirements are excluded. Preclinically, MSC-exosomal miR-145-5p suppressed TLR4/NF-κB signaling, reducing spinal IL-1β by 47% in SD rats. Schwann cell-exosomal MFG-E8 activated SOCS3/STAT3, increasing M2 macrophage CD206 by 63% and raising rat BBB scores by 3.8 points; Treg-exosomal miR-2861 upregulated tight junction proteins (occludin/ZO-1) to repair the blood-spinal cord barrier. Acupuncture (EA at GV14/GV4) upregulated spinal BDNF by 72% and NGF by 58% via Wnt/β-catenin, while EA at GV6/GV9 downregulated NLRP3 by 42-58% and TNF-α by 35-47%. Clinically, EA at EX-B2 increased ASIA scores by 3.2±1.1 points (Guo et al). Besides, 5x/week EA improved ASIA vs 3x/week (+6.4 points). EA+exercise reduced MAS by 1.6-2.9 points, with outcomes correlated to peripheral NLRP3 reduction, BDNF elevation, and MBI/WISCIII increases. Exosome cargo (miR-145-5p/MFG-E8) and NLRP3/BDNF are key regulatory molecules underlying acupuncture-mediated SCI recovery. However, limitations (small RCT samples, heterogeneous acupuncture protocols, unstandardized exosome isolation) hinder translation. Future work should focus on standardized biomarker detection, exosome engineering, and large-scale clinical trials. Show less

Blast-induced hearing loss (BIHL) is a major concern, particularly for military personnel, and is linked to impaired auditory neuron survival and synaptic plasticity. This study investigates the potential of the TrkB agonist 7,8-dihydroxyflavone (7,8-DHF) to reduce the severity of BIHL and promote recovery in a mouse model. Eight-week-old male C57BL/6J mice were used. A custom-built, compressed air-driven system utilizing a modified paintball apparatus was employed to deliver controlled unilateral double blasts (~22 psi exposure pressure) to the left ear. The blasts were administered 30 min apart. Immediately following the second blast, mice received either 7,8-DHF (10 mg/kg) or vehicle (10% DMSO) via intraperitoneal injection. Auditory brainstem responses (ABRs) were measured in both ears at baseline (pre-blast) and at several post-exposure time points. The consecutive blast exposure induced a significant elevation in ABR thresholds, indicative of hearing loss, in both the ipsilateral (exposed) and contralateral (unexposed) ears of vehicle-treated mice. Notably, mice treated with 7,8-DHF demonstrated a marked improvement in hearing recovery compared to the vehicle group. Significant reductions in ABR thresholds were observed in the ipsilateral ear at 4 weeks post-blast ( A controlled blast model demonstrates that systemic administration of the TrkB agonist 7,8-DHF exerts a protective effect, partially restoring auditory function after blast injury. This supports the therapeutic potential of targeting the BDNF-TrkB signaling pathway for managing BIHL. Show less

Intracerebral hemorrhage (ICH) is a devastating condition characterized by rapid onset, high rates of disability and mortality, and prolonged recovery. Dysregulated γ-aminobutyric acid type A receptor (GABAAR) signaling contributes to ICH-induced neurotoxicity, presenting a promising therapeutic target. To assess the neurorestorative effects of the GABAAR α1-selective partial positive allosteric modulator (PAM) CL218872 and the α5-selective negative allosteric modulator (NAM) MRK-016 on synaptic plasticity and neural repair following ICH. An ICH mouse model was constructed using collagenase IV, and ICH mice were administered the GABAAR modulators CL218872 or MRK-016. Differences in inflammation and neurological deficit score were compared between different groups of mice. Morphologic and functional changes in mouse neuronal cells were next determined by Nissl and Golgi-Cox staining. Synaptic structural changes in ICH mice were visualized by transmission electron microscopy, and changes in synaptic plasticity-related molecules were quantified to assess the effects of GABAAR modulators on synapses in ICH mice. Treatment with CL218872 resulted in a reduction in hemorrhage and improved neurobehavioral outcomes in ICH mice. Additionally, CL218872 mitigated inflammation by downregulating phospho-p65, IL-6 and TNF-α expression. Histological analysis revealed an increase in neuronal density, preservation of cell morphology, and enhanced synaptic connectivity following CL218872 treatment. Furthermore, synaptic structure was restored, and there was an upregulation of brain-derived neurotrophic factor (BDNF), growth-associated protein-43 (GAP-43), postsynaptic density protein 95 (PSD-95), and synaptophysin in ICH mice. However, treatment with MRK-016 yielded the opposite result. The GABAAR α1-selective PAM CL218872 exerts neuroprotective and neurorestorative effects in ICH, suggesting its therapeutic potential for ICH management. Show less

Persistent functional impairment and psychological distress are common after stroke, highlighting the need for effective post-discharge nursing strategies. We performed a retrospective cohort study evaluating the associations of a family-centered, new-media continuous nursing intervention on stroke recovery outcomes. The study included 107 patients with first-ever ischemic stroke who received either routine post-discharge care or a family-centered new-media continuous nursing intervention. Functional status, depressive symptoms, and quality of life were assessed at baseline and 6 months. Rehabilitation adherence, platform engagement indicators, and selected serum biomarkers related to neuroplasticity and inflammation were analyzed. Multivariable models were used to adjust for baseline clinical factors. At 6 months, the intervention group showed significantly greater improvements in Barthel Index scores, larger reductions in Patient Health Questionnaire-9 scores, and greater gains in quality of life compared with routine care. Rehabilitation compliance and medication adherence were higher in the intervention group. Within this group, greater platform engagement was associated with larger improvements in depressive symptoms and quality of life. In addition, patients receiving the intervention exhibited greater increases in serum brain-derived neurotrophic factor and endothelial progenitor cell counts, along with more pronounced reductions in IL-6 and TNF-α. Participation in the intervention remained independently associated with functional and psychological improvement after adjustment. Family-centered new-media continuous nursing is associated with improved functional independence, psychological recovery, adherence behaviors, and favorable biological changes in patients with ischemic stroke. Show less

Intermittent theta burst stimulation (iTBS) is increasingly explored as a non-invasive neuromodulatory approach capable of inducing long-lasting plasticity with potential therapeutic value in age-related neurological and psychiatric conditions. However, the cellular and molecular mechanisms underlying iTBS protocols remain largely unknown, limiting its further therapeutic development. Here, we investigated the behavioral, structural, synaptic, and calcium-dependent effects of a 7-day iTBS600 protocol using a combination of Prolonged iTBS did not alter general locomotor activity, anxiety-like behavior, or short-term recognition memory, indicating preserved baseline behavioral function. Despite the absence of behavioral changes, prolonged iTBS induced robust structural plasticity in hippocampal CA1 neurons, increasing total spine density and selectively enhancing the proportion of thin, learning spines. Synaptosomal analysis revealed upregulation of GluN1 and GluN2A, elevated BDNF levels, and activation of downstream Akt, ERK1/2, and mTOR pathways. Prolonged iTBS also enhanced perineuronal net formation around PV Together, these findings indicate that prolonged iTBS drives coordinated structural, synaptic, and Ca Show less

Cellular and synaptic plasticity in ventral tegmental area (VTA) play a key role in alcohol use disorder (AUD). Here, we first delineated the in vivo dynamics of dopamine (DA) neuron activity in VTA during chronic intermittent ethanol exposure: initial sensitization was followed by a phase of attenuated and dysregulated response upon the first high-concentration exposure, culminating in stable hyper-responsiveness. Chronic ethanol exposure impaired long-term potentiation of GABAergic synapses (LTP Show less

Job satisfaction is a critical factor influencing workplace efficiency and employee well-being. In the context of Industry 5.0 transformation, understanding the latent profiles of job satisfaction and their relationship with mental health outcomes, such as depression, anxiety, and digital-intelligence job insecurity, is critical for promoting employee well-being and organizational sustainability. This study aims to explore the latent profiles of job satisfaction among industrial workers and explore their associations with mental health outcomes. This study used cross-sectional data from 3,420 male frontline workers from a large automobile manufacturing enterprise in Jilin Province, China in April 2024. Latent profile analysis (LPA) was employed to identify distinct latent profiles of job satisfaction among industrial workers, while hierarchical linear regression analysis was used to analyze the relationship between job satisfaction and psychological health outcomes (depression, anxiety and digital-intelligence job insecurity). The score of job satisfaction among industrial workers in Jilin Province was 3.62 ± 0.90. Four profiles were identified: very low (5.97%), low-to-moderate (31.14%), moderately high (42.63%), and high job satisfaction (20.26%). Depression and anxiety showed a clear level-gradient pattern across profiles, whereas digital-intelligence job insecurity displayed a non-monotonic pattern with higher levels in the low-to-moderate and moderately high profiles. Work stress showed consistent associations with all outcomes, and job satisfaction profiles remained associated with depression and anxiety after covariate and stress adjustment; associations with digital-intelligence job insecurity were smaller but detectable. This study examined heterogeneity in job satisfaction among frontline industrial workers and its associations with mental health outcomes. Latent profile analysis identified four job satisfaction profiles. Job satisfaction profile membership remained strongly associated with depression and anxiety. Digital-intelligence job insecurity showed a non-monotonic pattern across profiles. These findings suggest that an individual-centered profile approach provides actionable differentiation of mental health symptom burden across distinct job satisfaction patterns, supporting more targeted workplace strategies. Show less

The objective of our investigation was to explore the features of gut microbiota dysbiosis and the concentrations of gut metabolites in relation to white matter injury (WMI). Furthermore, we sought to evaluate the influence of gut dysbiosis on neuroinflammation in WMI via intestinal metabolites, and its contribution to pathogenesis. A cerebral hypoxia-ischemia-induced WMI model was established in 3-day-old Sprague-Dawley rats. Liquid chromatography-mass spectrometry/gas chromatography-mass spectrometry analyses and 16S rRNA gene sequencing were undertaken to ascertain WMI biomarkers. Mechanistic experiments were used to analyse activation of the H3K9ac/BDNF/TrkB pathway and neuroinflammation. The analysis of 16S rRNA sequencing disclosed gut microbiota dysbiosis in WMI rats, quantified using linear discriminant analysis effect size. Overall, 341 differentially expressed metabolic markers between the WMI and Sham groups were discovered. The Kyoto Encyclopedia of Genes and Genomes network enhancement evaluation revealed significant downregulation of 20 metabolic processes in the WMI group, which is strongly related to changes in fecal microbial metabolites, and the synthesis process of unsaturated fatty acids was the most significant. Gut microbiota dysbiosis may influence WMI by downregulating metabolites such as eicosapentaenoic acid (EPA). Fecal microbiota transplantation increased EPA concentration in the brain tissue of WMI rats. Gut microbiota-derived EPA promoted H3K9ac and BDNF/TrkB expression and inhibited the transcription of pro-inflammatory TNF- WMI induces gut dysbiosis involving down-regulation of unsaturated fatty acid synthesis. Fecal microbiota transplantation leads to increased levels of EPA. Gut microbiota-derived EPA increases levels of acetylated histone H3K9ac, causes activation of the BDNF/TrkB pathway, reduces neuroinflammation, and improves WMI-associated myelination disorders. It provides a basis for targeted treatment of white matter injury in the future. Show less

To evaluate the predictive value of novel lipid parameters for coronary lesion severity in pCAD and to develop a nomogram-based prediction model. Patients newly diagnosed with pCAD at Qingdao Municipal Hospital (2021-2024) were enrolled and randomly assigned to training and validation cohorts in a 7:3 ratio. Coronary lesion severity was assessed using the Gensini score (GS), with patients stratified into mild or significant stenosis groups. Spearman correlation analysis was performed between GS and lipid parameters. Key predictors were selected using LASSO regression, and independent risk factors were identified by multivariable logistic regression to construct the nomogram model. The model's discrimination, calibration, and clinical utility were evaluated using receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA). Lp(a), non-HDL-C, RC, FFA, and BAR were positively correlated with GS (r = 0.34, 0.34, 0.18, 0.19, 0.18; all The proposed nomogram provides an effective tool for identifying pCAD patients with severe coronary artery stenosis, demonstrating robust predictive accuracy and potential clinical utility. Show less

Cadmium (Cd) is a potent neurotoxic heavy metal associated with cerebral oxidative disturbances. The beta-lactam antibiotic ceftriaxone has been known to modulate the expression of GLT-1, the primary glutamate transporter. This research has been framed to evaluate the potential neurodefensive activity of ceftriaxone against cadmium chloride (CdCl Show less

Subcutaneous fat deposition critically impacts duck meat quality and feed efficiency. We monitored growth and fat deposition in ducks from 30 to 70 days, performed transcriptomics on adipose tissue, and established an in vitro duck preadipocyte model to assess Fat deposition peaked at 50 days. Show less

In recent years, the global incidence of Non-Suicidal Self-Injury (NSSI) has risen, posing a significant challenge in public health. Adolescents are the main group affected. A cross-sectional study was conducted using a self-administered questionnaire to collect data from 6,311 adolescents in Hefei, China. This study employed the Compositional Isotemporal Substitution Model (CISM, a statistical method that estimates health effects of replacing time in one behavior with another while accounting for the interdependent, compositional nature of 24-h time-use data) to examine the impact of Screen Time (ST), Non-Screen-based Sedentary Time (NSST), Physical Activity, and Sleep Time on NSSI among adolescents. Compositional logistic regression analysis revealed that, relative to the remaining behavioral components, higher Light Physical Activity (LPA) ( The findings highlight those reasonably allocating adolescents' daily activities, reducing ST, can help lower the risk of NSSI among adolescents. Show less

Older adults increasingly rely on digital health resources, yet evidence regarding the relationship between eHealth literacy (eHL) and 24-hour movement behaviors (24-HMB), including physical activity (PA), sedentary behavior (SB), and sleep, remains underexplored. This study examined the associations between eHL and 24-HMB in Chinese older adults and examined self-efficacy as a potential mediator and moderator. Using a convenience sampling approach, 564 community-dwelling older adults (aged 60-74 years) were recruited from four urban Chinese cities via an online survey. A total of 553 valid cases were retained for analyses. eHL was assessed using the eHealth Literacy Scale-Web 3.0, and self-efficacy was assessed using a validated Self-Efficacy Scale. PA and SB were assessed objectively using ActiGraph GT3X+ accelerometers over three consecutive days (two weekdays and one weekend day). Sleep duration was derived from accelerometer-based estimates anchored by daily sleep logs. Multiple linear regression analyses were conducted to examine associations, and mediation and moderation were tested using PROCESS macro (Model 4 and Model 1, respectively), adjusting for age, sex, and education. After adjustment for covariates ( In this cross-sectional, urban, device-using sample of older adults, higher eHL was associated with a more favorable 24-HMB profile, particularly higher LPA and lower SB, while associations with sleep duration were weaker. Self-efficacy showed modest indirect associations consistent with partial mediation for PA and SB and also acted as a moderator of several associations. Given the observational design and modest effect sizes, findings should be interpreted cautiously and require confirmation in longitudinal or experimental studies with more representative sampling and improved sleep assessment. Show less

Intercellular communication is governed by the spatiotemporal dynamics of protein complexes at the cell-cell interface. However, conventional static interaction models fail to incorporate key physical constraints, such as steric hindrance, spatial compartmentalization, and dimensionality reduction that regulate complex assembly in vivo. To bridge the gap between static network topology and dynamic systems biology, we developed a multi-scale computational framework. We first identified a highly conserved, Fibroblast Growth Factor Receptor 1 (FGFR1)-centered cell adhesion and signaling motif by analyzing a diverse set of human cell-cell interfaces. We then constructed a multi-layer spatial stochastic simulator to recapitulate and interrogate the dynamic behavior of this network motif at cell-cell interfaces. Atomic-resolution structural models of the protein complexes within the motif were further generated using AlphaFold to define interaction rules for the stochastic simulations by categorizing binding interfaces. Our results show that the structural arrangement of cell-cell adhesion complexes controls how FGFR1 receptors cluster at the cell-cell interface, effectively dividing the membrane into distinct functional microdomains. Competition from decoy receptors further regulates this process by capturing receptors before they can participate in signaling. Even small changes in binding affinity can therefore alter receptor organization and disrupt normal signal transduction, which may contribute to human disease. By integrating macro-scale interactomics, atomic-level structural bioinformatics, and mesoscale stochastic modeling, this study reveals how structural interaction rules, combined with spatial constraints, shape the formation and function of intercellular signaling networks. Show less

Sleep deprivation (SD) impairs information processing through alterations of prefrontal cortex (PFC) function, yet the molecular underpinnings of this process remain poorly understood. We previously showed that SD disrupts sensorimotor gating by elevating prefrontal levels of the neurosteroid allopregnanolone (AP), a positive allosteric modulator of GABA-A receptors. Here we identify a complementary, mechanistically independent process whereby SD alters GABA-A currents in the PFC of mice and rats. SD reduced membrane expression of the chloride exporter KCC2, leading to intracellular chloride accumulation and a depolarizing shift in GABA-A receptor reversal potential that weakened GABAergic inhibition. Pharmacological normalization of chloride homeostasis with bumetanide fully rescued SD-induced deficits in sensorimotor gating and information encoding. SD also upregulated BDNF, and intra-PFC antagonism of its receptor TrkB restored KCC2 expression and normalized information processing, identifying BDNF-TrkB signaling as an upstream driver of chloride dysregulation. Notably, blocking AP synthesis rescued behavioral deficits without correcting chloride imbalance, confirming mechanistic independence. Finally, combined administration of AP and a KCC2 blocker produced information-processing deficits akin to those induced by SD. These findings identify TrkB-dependent disruption of prefrontal chloride homeostasis as a druggable mechanism underlying sleep loss-induced cognitive dysfunction. Show less

Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with a complex and not fully understood etiology. Increasing evidence suggests that neurotrophic factors involved in neurodevelopment and synaptic plasticity, as well as hormones of the hypothalamic-pituitary-adrenal (HPA) axis that regulate the stress response, may contribute to the pathophysiology of ADHD. This cross-sectional study aimed to compare children diagnosed with ADHD and healthy controls with respect to serum levels of brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neurotrophin-3 (NT-3), adrenocorticotropic hormone (ACTH), and cortisol. A total of 80 children aged 6-18 years with a diagnosis of ADHD and 81 healthy controls were included in the study. The severity of ADHD symptoms was assessed using the Conners' Parent Rating Scale-Short Version (CPRS-SV). Serum levels of biochemical parameters were measured using commercially available electrochemiluminescence immunoassay and enzyme-linked immunosorbent assay kits. Compared with the healthy control group, the ADHD group exhibited significantly higher serum levels of BDNF, GDNF, VEGF, ACTH, and cortisol, whereas NT-3 levels did not differ between the groups. These group differences remained statistically significant after controlling for potential confounding variables. Correlation analyses revealed no significant associations between neurotrophic factors, hypothalamic-pituitary-adrenal (HPA) axis hormones, and CPRS-SV subscale scores. The present findings indicate that neurotrophic factors and hormones related to the hypothalamic-pituitary-adrenal (HPA) axis are altered in medication-naïve children and adolescents with ADHD. The absence of a direct correlation between neurotrophic factors and HPA axis hormones suggests that these systems may contribute to the pathophysiology of ADHD through parallel yet partially independent and complex mechanisms. Future longitudinal and multimodal studies are warranted to elucidate the dynamic interactions between stress-related neuroendocrine processes and neurodevelopmental pathways in ADHD. Show less

This study aimed to identify distinct latent profiles (categories) of health behavior protection motivation among patients with type 2 diabetes using latent profile analysis. Subsequently, we compared e-health literacy levels across these patient categories and analyzed factors influencing protection motivation. The findings are intended to provide a scientific basis for precise diabetes management. From January to March 2025, a cross-sectional survey was conducted on a convenience sample of 253 patients, and data were collected using relevant scales such as the health-related behavior protection motivation assessment. LPA was performed using Mplus 8.3 to identify motivational profiles. Binary logistic regression was applied to determine influencing factors. A total of 253 valid questionnaires were collected. Two latent profiles of health-related behavioral protection motivation were identified: the "high perceived cost-incentive-dependent group" (n = 91, 35.97%) and the "high sensitivity-high efficacy group" (n = 162, 64.03%). The total eHealth literacy score of the "high perceived cost-incentive-dependent group" was 100.35 ± 17.89, which was significantly lower than that of the "high sensitivity-high efficacy group" (110.76 ± 13.78), with a statistically significant difference (t = -5.165, P < 0.001). Logistic regression analysis revealed that patients who monitored their blood glucose more than three times per week were 2.95 times more likely to have a higher level of protective motivation compared to those who did so three times or fewer (95% CI: 1.679-5.197, P < 0.001). There is population heterogeneity in health-related behavioral protection motivation among patients with type 2 diabetes. Frequency of blood glucose monitoring per week was identified as influencing factors of motivational profile membership. Differences in eHealth literacy levels were also observed between the two groups. Targeted interventions should be provided based on population characteristics to enhance motivation, improve electronic health literacy, and behavioral compliance. Show less

Pesticides are essential for modern agriculture but raise concerns about potential neurodevelopmental consequences, leading to bans in some countries. This study aimed to investigate the long-term effects of prenatal exposure to chlorpyrifos (CPF) on behavior and DNA methylation, considering genetic susceptibility via the apolipoprotein E ( Show less

Psilocybin is studied as innovative medication in anxiety, substance abuse and treatment-resistant depression. Animal studies show that psychedelics promote neuronal plasticity by strengthening synaptic responses and protein synthesis. However, the exact molecular and cellular changes induced by psilocybin in the human brain are not known. Here, we treated human cortical neurons derived from induced pluripotent stem cells with the 5-HT2A receptor agonist psilocin - the psychoactive metabolite of psilocybin. We analyzed how exposure to psilocin affects gene expression, neuronal morphology, synaptic markers and neuronal function. Psilocin provoked a 5-HT2A-R-mediated augmentation of BDNF abundance. Transcriptomic profiling identified gene expression signatures priming neurons to neuroplasticity. On a morphological level, psilocin induced enhanced neuronal complexity and increased expression of synaptic proteins, in particular in the postsynaptic compartment. Consistently, we observed an increased excitability and enhanced synaptic network activity in neurons treated with psilocin. In conclusion, exposure of human neurons to psilocin might induce a state of enhanced neuronal plasticity, which could explain why psilocin is beneficial in the treatment of neuropsychiatric disorders where synaptic dysfunctions are discussed. Show less

Methadone maintenance treatment (MMT) is one of the major pharmacotherapies for opioid use disorder. The underlying mechanisms of addiction and the treatment response are only partially understood. The study's main goal was to identify differential DNA CpG methylation that occurred in response to MMT. Toward this goal, we have conducted a longitudinal epigenome-wide study of blood samples from 64 patients at the beginning and after 1-3 years of MMT, using a linear mixed model. A total of 1881 differentially methylated probes (DMPs) were identified (FDR < 0.05), controlling for sex, age, estimates of blood cell proportions, and the first two principal components based on genome-wide SNP genotypes. Among the genes annotated to the top DMPs are The study provides preliminary insight into the epigenetic effect of MMT. Future studies will have to confirm the DMPs, assess their impact on gene expression, and determine their clinical relevance. Show less

Exercise as a non-pharmacological measure is important to increase the brain plasticity hence improving cognitive performance as well as mental health. This narrative review describes in depth the hierarchical multiscale processes of neuroplasticity to exercise, including the presence of neurotrophic factor regulation, cellular metabolic adaptations and neurotransmitter remodeling, up to the structure and functional reorganization of brain networks as seen through neuroimaging, and concluding with adaptive cognitive and behavioral outcomes. We further investigate the role of personal variations in genetic time and social environments in moderating the neuroplasticity of exercise. Furthermore, the review identifies the importance of combining multimodal visualization methods with computational models in generating accurate workout prescriptions and their potential of translation into clinical and educational practice. Lastly, the research problems and "grand challenges" are addressed, with a focus on the importance of exercise as a pleiotropic behavior-intervention and its general implications to the area of promoting brain health. Show less

Major depressive disorder (MDD) is a highly prevalent psychiatric illness for which rapid-acting antidepressants such as ketamine provide only transient benefit. Because κ-opioid receptor (KOR) signaling contributes to stress-related dysphoria and impaired neuroplasticity, we examined whether KOR antagonism could prolong ketamine's antidepressant-like effects in a mouse model of adolescent chronic unpredictable stress (CUS). Male Show less