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Alzheimer's Disease (AD) incidence and prevalence increase every year, commonly related to neuron inflammation and degeneration conditions. Tempeh, a traditional fermented product from Indonesia, was reported to have anti-inflammatory, antioxidant, and anti-Alzheimer properties. However, anti-Alzheimer properties of tempeh peptide extracts have not been extensively examined. This research studied the effect of the extracted peptide from tempeh in preventing and delaying Alzheimer's disease. Tempeh peptide was extracted using water maceration and quantified using HPLC and spectrophotometry. Anti-Alzheimer properties of tempeh were analyzed with Ellman's assay of anticholinesterase and in vitro gene expression analysis using LPS-induced neural Schwann cells. As a result, tempeh contained 19.27% of GABA, which is reported to have anti-Alzheimer properties, and other amino acids. Tempeh peptide extract at 12.5 µg/mL had strong inhibition activity toward acetylcholinesterase at 12.61%, and 100 µg/mL of tempeh peptide extract had 8.97% butyrylcholinesterase inhibition activity. Tempeh peptides extract also altered the expression of various genes related to Alzheimer's disease, such as TNF-α, BACE 1, Ntrk 1, BDNF 2, and APP. This research proved that various peptides from tempeh have anti-Alzheimer properties. Show less

We aimed to delineate strategies for improved management of brain metastases (BM) in breast cancer by investigating the estrogen-related BDNF–TrkB pathway within the tumor microenvironment. Surgical specimens of BM tissues from breast cancer patients were analyzed using multiplex immunohistochemistry. Expression patterns of BDNF, TrkB, and phospho-AKT were assessed separately in tumor and stromal compartments and compared across molecular subtypes. Clinical data were reviewed to identify factors associated with brain-specific progression-free survival (BPFS) and overall survival (BOS). Endocrine therapy following BM diagnosis was independently associated with prolonged brain-specific survival among luminal patients (HR for BPFS and BOS, 0.22 and 0.19; Survival after BM was influenced by both tumor characteristics and treatment modalities. In luminal disease, endocrine therapy and estrogen depletion may exert anti-tumor activity through inhibition of the BDNF–TrkB pathway. These findings provide novel insight into the biology of breast cancer brain metastases and suggest a rationale for further validation in multicenter studies. Not applicable. The online version contains supplementary material available at 10.1007/s11060-025-05393-3. Show less

Chronic alcohol drinking increases susceptibility to cognitive impairment; however, the underlying mechanisms remain unclear. In this study, we investigated the effects of chronic alcohol drinking on working and recognition memory in a Marchigian Sardinian alcohol-preferring (msP) rat line. Due to interest in insulin-based medications for alcohol use disorder, we examined insulin/insulin-like growth factor 1 (IGF-1) genes in the prelimbic (PL) and infralimbic (IL) medial prefrontal cortex, a region linked to alcohol dependence and cognition. Male and female msPs received access to alcohol (20% v/v) and water (H Show less

Jiaotaiwan (JTW) is a classic traditional Chinese medicine (TCM) prescription for treating depression, but its potential mechanisms are not fully understood. The aim of this study is to detect the levels of serum Short-chain fatty acids (SCFAs) and cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA)-cAMP-response element binding protein (CREB)-brain derived neurotrophic factor (BDNF) signaling pathway, further revealing the scientific connotation of the antidepressant effect of JTW. In this multicenter, randomized, controlled study, 120 patients with depression were divided into the JTW (16.5 g/d) group, JTW (16.5 g/d) + selective serotonin reuptake inhibitors (SSRIs) group, and SSRIs group. Hamilton depression Scale-24 (HAMD-24) and Self-rating depression scale (SDS) were used for efficacy evaluation. Enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) were used to evaluate the expression levels of cAMP-PKA-CREB-BDNF signaling pathway. Serum SCFAs concentrations were analyzed using liquid chromatograph-mass spectrometer (LC-MS) targeted metabolomics. After eight weeks of treatment, HAMD score and SDS score were significantly decreased in the three groups, and HAMD score in JTW + SSRIs group was significantly lower than that in SSRIs group. After treatment, the expression levels of cAMP-PKA-CREB-BDNF signaling pathway were significantly increased in the three group, with the JTW + SSRIs group showing more significant increase. After treatment, the levels of isobutyric, butyric, isovaleric, and valeric acids in the JTW + SSRIs groups were significantly higher than that before treatment, and the levels of isobutyric, and isovaleric acids in the JTW + SSRIs group was significantly higher than that in the JTW group and SSRIs groups. JTW can alleviate symptoms in patients with depression, and its antidepressant mechanism may be related to regulating serum SCFAs and cAMP-PKA-CREB-BDNF signaling pathway. Show less

This study aimed to comprehensively evaluate the clinical effectiveness and safety of acupuncture combined with repetitive transcranial magnetic stimulation (rTMS) in treating post-stroke cognitive impairment (PSCI) through meta-analysis and trial sequential analysis (TSA), moreover to provide an evidence-based basis for the treatment of PSCI in clinical practice. The study conducted a comprehensive search of eight major domestic and international databases, including PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP and China Biology Medicine (CBM). Four English and four Chinese databases of randomized controlled trials of acupuncture combined with rTMS for the treatment of PSCI from inception until July 2025. Systematic reviews and meta-analyses were conducted based on the Cochrane systematic review method by using RevMan5.4 and Stata/MP 18.0, and trial sequential analyses were performed by TSA 0.9. Sixteen RCTs involving 1,058 patients were included, including 532 patients in the experimental group and 526 patients in the control group. Meta-analysis results showed that the experimental group had a higher clinical effectiveness rate in treating patients with PSCI compared to the control group [RR = 1.29, 95% CI (1.08, 1.55), Acupuncture combined with rTMS can improve cognitive function, regulate daily living ability, and regulate neurotransmitter levels in patients with PSCI, which is worthy recommended in the clinic. However, due to limitations in sample size, inclusion quality and incomplete reporting, it is worth noting that more rigorously designed and high-quality studies are needed to further validate these conclusions. Show less

This review examines the existing literature on the structural and functional changes in the anatomy of the prefrontal cortex (PFC) associated with autism spectrum disorder (ASD), focusing on the roles of molecular signaling disruptions and trace element imbalances. A literature review was performed through a structured search of academic publications from 2010 to 2025. Anatomic variations and structural and functional abnormalities within the PFC, including disruptions in neural connectivity, synaptic plasticity, and neurochemical balance, significantly contribute to the cognitive, social, and emotional deficits observed in ASD. The interplay between brain-derived neurotrophic factor dysregulation, oxidative stress, and trace element imbalances further exacerbates these dysfunctions. According to our findings, the anatomy of the PFC appears to play a crucial role in the pathophysiology of ASD, given its involvement in executive function, emotional processing, and social cognition, suggesting a multifactorial pathophysiology that demands a multidimensional research approach. Show less

To investigate the role of BDNF/TrkB signaling in Central Post-Stroke Pain (CPSP) and to investigate whether this signaling is related to the analgesic effect of optogenetics. This study was conducted in two parts. First, 40 rats were acquired and randomly divided into four groups: Sham, CPSP, CPSP + ANA-12 (inhibitor of the BDNF/TrkB signaling pathway), and CPSP + 1% DMSO. The Sham group received a saline injection into the Ventral Posterolateral Nucleus of the Thalamus (VPL), whereas the other three groups were injected with type IV collagenase. Additionally, the two groups of CPSP rats were separately injected with ANA-12 or 1% DMSO in the VPL. Second, 50 rats were acquired and randomly divided into five groups: Sham, CPSP, CPSP + NpHR, CPSP + NpHR + BDNF, and CPSP + NpHR + PBS. From day 3 after collagenase injection, rats in the three NpHR groups received yellow laser stimulation at a wavelength of 589 nm six times a day for 12 consecutive days. Subsequently, two groups of stimulated rats were separately injected with BDNF or PBS in the VPL. Optogenetic therapy effectiveness and potential mechanisms were evaluated using pain threshold tests and molecular biology, among other methods. According to the pain threshold test results, optogenetic therapy and ANA-12 injection reversed aberrant CPSP while downregulating BDNF and TrkB. Conversely, exogenous BDNF injection reversed the therapeutic effect of optogenetics on pain. The BDNF/TrkB signaling pathway in the ascending pain modulation system may crucially modulate CPSP in rats. Furthermore, optogenetic therapy could suppress BDNF/TrkB signaling in the ascending pain modulation system, potentially alleviating thalamic hemorrhage-induced Neuropathic Pain (NP). Show less

The 808-nm wavelength laser has emerged as a promising non-invasive tool with significant therapeutic potential in various medical fields. This review highlights its biological mechanisms, including anti-inflammatory effects, tissue repair, and pain modulation. The laser inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, reducing pro-inflammatory cytokines (e.g., tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6)) and increasing interleukin-10 (IL-10), an anti-inflammatory mediator that accelerates healing. The laser also activates the transforming growth factor-beta (TGF-β) pathway to stimulate collagen synthesis and fibroblast activity, enhancing tissue regeneration. Additionally, by promoting vascular endothelial growth factor (VEGF) expression, and improves neovascularization and tissue oxygenation as well. The modulation of transient receptor potential vanilloid 1 (TRPV1) channels, increased adenosine triphosphate (ATP) production, and activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) and the brain-derived neurotrophic factor (BDNF) pathways further support neuroprotection and cellular recovery. Importantly, recent insights suggest the laser's interaction with glial cells particularly astrocytes and microglia plays a critical role in managing neuro-inflammation and improving outcomes in neurological disorders such as hydrocephalus. The ability to influence cerebrospinal fluid regulation and enhance brain barrier permeability positions the 808-nm laser as a potential therapeutic option for improving life quality in affected individuals. Despite its potential, further clinical studies are required to validate and standardize its application across medical protocols. Show less

This research aimed to explore the serum levels of calcium/calmodulin-dependent protein kinase II (CaMKII) in hyperventilation syndrome (HVS) patients and its correlation with psychological disorders. This prospective observational study enrolled 168 HVS patients who came to our hospital from February 2021 to January 2023. The serum CaMKII, 5-hydroxytryptamine (5-HT), and brain-derived neurotrophic factor (BDNF) levels were measured by enzyme-linked immunosorbent assay method. Hamilton depression rating scale was used to assess the depression status of all study subjects. Hamilton anxiety rating scale, the self-rating anxiety scale, and the self-rating depression scale were used to further evaluate the psychological status of all patients. The self-rating depression scale, Hamilton anxiety rating scale, and self-rating anxiety scale scores in the depression group were significantly elevated compared to the non-depression group (P < .05). The serum CaMKII, 5-HT, and BDNF levels were significantly declined in the depression group compared to the non-depression group. Pearson analysis showed a positive correlation among CaMKII levels, 5-HT levels, and BDNF levels. Serum levels of CaMKII were associated with the psychological status of HVS patients (depression and anxiety). CaMKII could be used to predict depression in HVS patients. CaMKII was a risk factor for depression in HVS patients. This study showed that the serum CaMKII levels decreased in HVS patients with depression. The serum CaMKII level was correlated with 5-HT, BDNF and could be used to predict depression in HVS patients. Show less

To evaluate the relationship between the levels of interleukin (IL)-6 (a marker of inflammation), cortisol (a marker of the hypothalamic-pituitary-adrenal axis functioning), and brain-derived neurotrophic factor (BDNF, a key neurotrophic factor) in acute and long-term (after 1 month) periods of traumatic brain injury (TBI) with trauma characteristics, as well as neurological and mental disorders. Analysis of data from a cohort longitudinal prospective study. Changes over time in IL-6, cortisol, and BDNF levels during the 1 month after injury were described: IL-6 and cortisol decreased, while BDNF increased, reflecting mechanisms of primary injury and secondary recovery processes. In the acute period, levels of IL-6, cortisol, and BDNF correlated with the severity of the patient's condition: low BDNF and high IL-6 and cortisol levels were associated with a more severe injury, as assessed by the Glasgow Coma Scale. An association between these markers and the presence of amnesia and abnormal EEG changes in the acute period of TBI was found. IL-6, cortisol, and BDNF are important pathophysiological markers of TBI associated with both immediate features of TBI and its complications. Show less

To explore the molecular mechanisms underlying clozapine-induced metabolic syndrome (MetS) in schizophrenia patients, providing scientific evidence for clinicians to prevent and manage metabolic syndrome during the treatment of psychiatric disorders. Ten schizophrenia patients with MetS and ten matched controls were recruited from Shanghai Mental Health Center according to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for schizophrenia and the 2016 Chinese Adult Dyslipidemia Prevention and Treatment Guidelines for MetS. Peripheral blood RNA sequencing was performed to identify differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) network were used to pinpoint hub genes. Mendelian randomization (MR) was conducted to validate causal relationship between serum brain-derived neurotrophic factor (BDNF) levels and MetS components. A total of 1019 DEGs were identified, grouped into eight mRNA modules through WGCNA. Key hub genes included Significant differences in gene expression are observed between schizophrenia patients with and without MetS. Individual variability in clozapine-induced MetS may be linked to DEGs. Show less

Post-stroke depression (PSD) is a common and clinically significant complication of stroke, associated with worse rehabilitation potential and increased mortality risk. The prevalence of PSD varies from 25% to 59%, depending on the duration of follow-up, peaking in the first years after the stroke event. The pathogenesis of PSD results from a complex interplay of biological and psychological factors, extending far beyond monoamine deficiency. Key roles are played by damage to monoaminergic pathways, neuroinflammation, dysfunction of the hypothalamic-pituitary-adrenal axis, reduced neuroplasticity (including BDNF deficit), and impaired integrity of neuronal networks. The clinical picture is characterized by a complex of affective (apathy, anhedonia), cognitive (executive dysfunction), and dyssomnic disorders. Although selective serotonin reuptake inhibitors remain the first-line treatment, the modern therapeutic approach to PSD requires targeting all components of its pathogenesis. A promising direction is the use of antidepressants with a multimodal mechanism of action, such as the original drug fluvoxamine, which combines serotonergic effects with anti-inflammatory and neuroprotective properties via sigma-1 (σ1) receptor agonism. Optimizing PSD treatment is achievable through the implementation of a personalized approach, including long-term screening and comprehensive management of the identified disorders. Show less

Chronic pain and opioid use disorder (OUD) are highly prevalent and frequently co-occurring conditions that pose complex treatment challenges. While opioids are effective for pain management, prolonged use significantly enhances risk of developing substance dependence. Conversely, addiction-focused therapies often fail to relieve persistent somatic pain. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has emerged as a novel adjunctive treatment with potential to address chronic pain and substance use disorders concurrently. The present investigation examines the role of intravenous ketamine infusions in cases with coexisting chronic pain and OUD. It explores pharmacological mechanisms, therapeutic applications, clinical efficacy, and safety considerations of ketamine. Ketamine primarily acts by blocking NMDA receptors, which are central to glutamatergic signaling. This inhibition reduces neural excitability and promotes neuroplastic changes, including upregulation of brain-derived neurotrophic factor (BDNF), a protein associated with synaptic remodeling and recovery within pain and addiction pathways. These mechanisms are likely to contribute to ketamine mediated dual efficacy in managing nociceptive symptoms and reducing opioid dependence. Clinical studies suggest that ketamine may reduce pain severity, decrease opioid consumption, and alleviate withdrawal symptoms in select populations. While early evidence supports ketamine's use, its side effect profile, including dissociative symptoms, sympathomimetic activity, and potential for misuse, necessitates careful patient selection, monitoring, and oversight. Evidence remains limited by inadequate sample sizes, non-standardized protocols, and short follow-up periods. Despite these limitations, ketamine remains a promising adjunct in multimodal care, especially when conventional therapies are ineffective. Ongoing research is essential to refine protocols and to explore integration with behavioral and pharmacologic addiction interventions. Show less

This study aimed to determine whether a history of childhood abuse (CA) and baseline serum brain-derived neurotrophic factor (sBDNF) levels predict remission at 12 weeks and 12 months in patients with depressive disorders, and to examine potential interactions between these factors. A total of 1,086 patients with depressive disorders, participating in a naturalistic, stepwise antidepressant treatment study, were assessed at baseline. CA was evaluated using the Nemesis Childhood Trauma Interview, and sBDNF levels were measured. Remission was defined as a Hamilton Depression Rating Scale score of ≤ 7. Logistic regression analyses examined the independent and interactive effects of CA and sBDNF on remission outcomes, adjusting for relevant covariates. Low baseline sBDNF independently predicted poorer remission at 12 months (p = 0.045) but not at 12 weeks (p = 0.720). In adjusted analyses, CA alone did not significantly predict remission at either time point (all p > 0.05). However, patients who had both a CA history and low baseline sBDNF showed significantly lower remission rates at 12 weeks (p = 0.018) and 12 months (p = 0.009), indicating a significant interaction between these factors. These findings underscore the importance of integrating psychosocial and biological factors in personalized depression treatment. Routine screening for childhood trauma, combined with assessment of sBDNF levels, may help identify high-risk patients needing targeted interventions. Further prospective research is necessary to validate these findings. Show less

Exploding head syndrome (EHS) is a parasomnia characterized by the perception of loud noises originating from inside the head during sleep transitions, often accompanied by visual phenomena and fear. Treatment remains challenging due to unknown etiology and limited therapeutic options. We report a 75-year-old man with chronic exploding head syndrome experiencing lightning-like sensations, thunder-like sounds, sleep paralysis, and intense fear during sleep onset. Episodes occurred multiple times weekly for over five years. Initial treatments, including gabapentin, valproic acid, amitriptyline, and buspirone, proved ineffective. The patient was subsequently treated with sublingual ketamine, starting at 25 mg every third night and escalating to nightly dosing. After one month, episode frequency decreased from 3-4 times weekly to once every two weeks. By three months, episodes occurred monthly with reduced intensity. After six months, the patient experienced only occasional sleep paralysis with the complete resolution of exploding head syndrome and reported improved quality of life. Ketamine's mechanism likely involves N-methyl-D-aspartate (NMDA) receptor modulation, brain-derived neurotrophic factor release, and σ1 receptor agonism, promoting neuroplasticity and sleep regulation. This case represents a reported successful treatment of exploding head syndrome with ketamine, suggesting a potential therapeutic approach for this refractory parasomnia. Further studies are warranted to evaluate ketamine's efficacy in exploding head syndrome treatment. Show less

Axon growth is an essential cellular process during neural development, and its dysregulation contributes to numerous neurodevelopmental disorders. During axon growth, extracellular signals direct neurons to extend projections that connect with their synaptic targets. Paxillin is a key member of adhesion sites that control motility by linking the intracellular actin cytoskeleton to the extracellular matrix. Paxillin also binds to the cytoskeletal protein, tubulin. However, little is known about the role of adhesion proteins in neurons. Here, we use conditional paxillin knockout mice to investigate how loss of paxillin in pyramidal cortical neurons affects developing neuron morphology. Surprisingly, loss of paxillin in pyramidal cortical neurons caused no change in axon length or soma area between control ( Show less

Neurodegenerative diseases (NDs) such as Alzheimer's disease (AD) and Parkinson's disease (PD) represent a growing global health concern with no definitive cure. Increasing evidence suggests that mind-body practices like yoga may offer neuroprotective benefits by modulating stress, neuroinflammation, and neuroplasticity. This narrative review explores the clinical outcomes, mechanistic insights, and biomarker evidence supporting yoga as a therapeutic intervention for AD and PD. Different studies indicate that regular yoga improves motor and cognitive functions, mood, and quality of life in affected individuals. At the molecular level, yoga enhances neurotrophic factors such as brain-derived neurotrophic factor (BDNF), reduces pro-inflammatory cytokines (e.g., IL-6, TNF-α), mitigates oxidative stress, and may preserve gray matter volume in key brain regions. These findings support the hypothesis that yoga induces favorable neuroplastic adaptations that may slow neurodegeneration. Despite encouraging early results, heterogeneity in study design, intervention duration, and sample size issues have limited the incorporation of neuroimaging and biomarker endpoints, which means further studies are warranted to clarify yoga's therapeutic potential and mechanism in ND management. Show less

The onset of puberty is a critical developmental milestone regulated by complex neuroendocrine networks that integrate genetic, metabolic, and environmental cues. Among the molecular systems coordinating this transition, neurotrophins-including brain-derived neurotrophic factor (BDNF), nerve growth factor, neurotrophin-3, and neurotrophin-4/5-have emerged as important modulators of hypothalamic maturation and the activation of gonadotropin-releasing hormone (GnRH) neurons. Beyond their established roles in neuronal survival and differentiation, neurotrophins contribute to hypothalamic circuit plasticity, influence GnRH neuronal activity, and participate in the integration of metabolic and environmental signals relevant to reproductive maturation. Experimental studies, primarily based on animal and cellular models, demonstrate that BDNF and its receptor play a role in normal pubertal onset, whereas disruptions in neurotrophin signaling have been implicated in central precocious puberty, delayed puberty, and hypogonadotropic hypogonadism. In humans, available evidence is more limited and derives mainly from genetic studies, circulating neurotrophin measurements, and clinical observations. This review provides an integrative synthesis of current experimental and clinical data on neurotrophin-mediated regulation of pubertal timing, highlighting both physiological mechanisms and pathological conditions. While neurotrophins represent promising modulators at the intersection of neurodevelopment, metabolism, and reproduction, further longitudinal and translational human studies are required to define their diagnostic and therapeutic potential in pediatric endocrinology. Show less

Short sleep duraiton is a putative risk for dementia, whereas midlife obesity is an well-known risk factor. Midlife short sleep and obesity share some biological changes such as inflammations or metabolic changes, but their combined impact is not yet fully understood. Our aim is to investigate the associations of short leep obesity with cognitive decline and dementia risk, and to investigate whether these associations are mediated by blood markers. This is an analysis of prospective cohort study of adults who were free of dementia, had data on sleep duration and BMI at baseline in 1997-1999, and were tracked for dementia diagnoses until 2023 via linkage to electronic health records. Participants will be divided into four groups: (1) the reference group (2) short sleep (2) short sleep (≤6 hours) and non-obese weight; (3) normal sleep and obesity (≥30kg/m Show less

Early identification of individuals at risk for cognitive impairment is essential for timely intervention and public health planning. While sociodemographic and clinical predictors are well recognized, the role of nutrition and its interactions in cognitive health remains less explored. Using data from the 2011-2014 National Health and Nutrition Examination Survey (NHANES, Ensemble models demonstrated excellent predictive performance, consistently outperforming traditional classifiers. Key predictors included education, age, socioeconomic status, and chronic disease conditions. Among nutritional factors, vitamin B2 emerged as consistently associated with lower predicted cognitive impairment risk across all three models, with notable interactions observed with copper and vitamin E. Exploratory Interpretable machine learning models integrating cognitive tests with demographic, clinical, and nutritional variables can accurately predict cognitive impairment. Nutritional predictors, particularly vitamin B2 and its interactions, may contribute to model performance and biological plausibility, suggesting potential avenues for stratified monitoring strategies. Show less

Sarcopenia is a progressive, age-related loss of skeletal muscle mass, strength, and function, strongly associated with frailty, disability, and chronic disease. Its pathogenesis involves chronic low-grade inflammation, hormonal imbalance, and impaired anabolic signaling, making biomarkers essential for diagnosis, prognosis, and intervention monitoring. This review systematically analyzes randomized controlled trials (RCTs) evaluating the impact of physical exercise on biomarkers relevant to sarcopenia. Exercise modulates both pro-inflammatory markers (e.g., IL-6, TNF-α, CRP) and anti-inflammatory cytokines (e.g., IL-10, IL-15), while also affecting growth factors like IGF-1, myostatin, and follistatin. These changes support muscle anabolism, reduce catabolic signaling, and improve physical performance. In addition, we highlight a growing class of emerging exerkines, including irisin, apelin, beta-aminoisobutyric acid (BAIBA), decorin, brain-derived neurotrophic factor (BDNF), and meteorin-like factor (Metrnl). These molecules exhibit promising roles in mitochondrial health, lipid metabolism, muscle regeneration, and immune modulation, key processes in combating inflamm-aging and sarcopenic decline. Despite encouraging findings, biomarker responses remain heterogeneous across studies, limiting translational application. The integration of biomarker profiling with exercise prescription holds the potential to personalize interventions and guide precision medicine approaches in sarcopenia management. Future large-scale, standardized trials are needed to validate these biomarkers and optimize exercise protocols for aging populations. Show less

Aquatic species are exposed to several long-chain per- and polyfluoroalkyl substances (PFASs) in the environment but their potential toxicity is not well studied. In this study, we assessed the effects of perfluoroundecanoic acid (PFUnDA) exposure on developing zebrafish. To do this, we investigated the potential for oxidative stress and neurotoxicity by measuring reactive oxygen species, apoptosis, gene expression, and locomotor activity. Mortality was evident in fish exposed to 1000 µg/L PFUnDA, and apoptosis was indicated in fish exposed to 100 µg/L PFUnDA via an increase in Show less

Non-invasive brain stimulation (NIBS) techniques-including repetitive transcranial magnetic stimulation (rTMS), theta-burst stimulation (TBS), paired associative stimulation (PAS), transcranial direct current stimulation (tDCS), and transcranial alternating current stimulation (tACS)-have emerged as valuable tools for modulating neural activity and promoting plasticity. Traditionally, their effects have been interpreted within a binary framework of long-term potentiation (LTP)-like and long-term depression (LTD)-like plasticity, largely inferred from changes in motor evoked potentials (MEPs). However, existing models do not fully capture the complexity of the biological processes engaged by these techniques and despite extensive clinical application, the cellular and molecular mechanisms underlying NIBS remain only partially understood. This systematic review, conducted in accordance with the PRISMA 2020 guidelines, synthesizes evidence from in vivo, in vitro, and ex vivo studies to delineate how NIBS influences neurotransmission through intracellular signaling, gene expression, and protein synthesis at the cellular level. Emphasis is placed on the roles of classical synaptic models, grounded in Ca Show less

Since there is currently no cure for Parkinson's disease, pharmacobiotic approaches based on gut microbiota-capable of producing pharmacologically active compounds-are under development. In this study, we propose LfU21, derived from the strain Show less

Chronic stress disrupts neuroendocrine regulation, neurotransmitter balance, and neuronal redox homeostasis, thereby contributing to the development of anxiety-related neuropathology. Arecoline, the predominant alkaloid of Show less