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We investigated the relationship between cerebrospinal fluid (CSF) and plasma biomarkers of inflammation, neurodegeneration, and neurocognitive performance in people with HIV (PWH), using longitudinal samples from two previously published cohorts: ACTG A5090 (virally suppressed on antiretroviral therapy, ART) and A736 (ART-naïve or failing). We analyzed paired CSF and plasma samples, as well as 7-domain standardized neurocognitive test scores, at baseline and 24 weeks. Biomarkers included markers of inflammation (e.g., TNF-α, IL-6, IP-10) and neurodegeneration (e.g., NFL, p-Tau217, Aβ42), which were quantified via high-sensitivity immunoassays. Associations with cognition were tested using regression, mediation, and interaction models. Cross-sectional analyses revealed nominal associations between inflammatory markers and cognitive performance, with plasma IL-6 and IP-10 at baseline, and CSF TNFα at week 24 showing the strongest correlations (p < 0.05, uncorrected); however, none survived correction for multiple comparisons. Conversely, higher CSF Aβ42 and plasma BDNF were positively associated with memory and executive function. Longitudinally, biomarker changes did not significantly predict change in global cognition (ΔNPZ-8); the strongest trend (p-Tau217, ρ = -0.12, p = 0.38) was not statistically significant, and multivariate models failed to identify robust predictors (R These results suggest a potential role of CSF TNFα in mediating the neurocognitive effects of HIV and highlight compartment-specific inflammatory dynamics. Plasma TNFα, GFAP, and NFL may serve as peripheral indicators of CNS pathology, though with only moderate concordance. Astrocyte-tau interactions require cautious interpretation pending replication in larger cohorts. Show less

Sleep and physical activity are modifiable behaviours linked to pain. Sleep disturbance often co-occurs with persistent pain and may contribute to its development. Exercise is a first-line treatment for chronic pain. Previous work showed that sleep disturbance worsens and prolongs postinjury pain behaviours, exercise mitigates these effects, and brain-derived neurotrophic factor may play a mechanistic role. Deeper insight requires a broader assessment of pain behaviours and systemic biomarkers related to inflammation, tissue repair, and neuromodulation. This study addresses these gaps. Twenty-nine adult female Sprague-Dawley rats performed an intensive lever-pulling task for 4 weeks to induce overuse injury and then underwent one of three 4-week interventions: intermittent sleep disturbance, voluntary exercise (via access to a running wheel), or both. Pain-related behaviours and 71 blood analytes were measured immediately preinjury, postinjury, and postintervention. Overuse injury decreased grip strength and increased mechanical sensitivity in the injured forepaws. After cessation of the injury inducing task, these changes persisted with sleep disturbance but recovered to, or exceeded, preinjury levels with exercise, even with concurrent sleep disturbance. Biomarker analyses revealed distinct neuroimmune responses to injury and sleep disturbance, particularly mediators of inflammation and neuroplasticity, that were offset by exercise. Correlations between biomarkers and behavioural outcomes support mechanistic links between injury, sleep, exercise, and recovery. Findings demonstrate that postinjury sleep disturbance induces neuroimmune changes that increase persistent pain vulnerability, whereas aerobic exercise counters these effects. This highlights the interaction between sleep and exercise in recovery and their potential as strategies to prevent and manage chronic pain. Show less

Despite advances in acute ischemic stroke (AIS) research, identifying reliable biomarkers and regulatory mechanisms remains challenging. We first identified AIS-related genes via extensive literature review, retrieved dataset GSE16561 from the Gene Expression Omnibus (GEO, https://ncbi.nlm.nih.gov/geo/), and performed differential/enrichment analyses. Bioinformatics verified N6-methyladenosine (m Show less

Chemotherapy-related cognitive impairment (CRCI) is a prevalent and distressing issue among older adults with cancer, affecting quality of life and treatment adherence. While its mechanisms remain unclear, biomarkers have emerged as promising tools for understanding CRCI. This systematic review aimed to explore the relationships between cognitive impairment following chemotherapy and biomarkers in older patients with cancer. A comprehensive search was conducted through December 2024 across PubMed, CINAHL, Embase, PsycINFO, and the Cochrane Library. An additional hand search was performed through July 2025. The focus was on patients over 60 years old with chemotherapy-related cognitive impairment and associated biomarkers. The review adhered to PRISMA 2020 guidelines, and the methodological quality of included studies was assessed using the Joanna Briggs Institute checklist to ensure rigor and reliability. Six of the initial 6,324 articles met the inclusion criteria, and seven additional studies were identified through manual searching. In total, 13 studies identified several biomarkers associated with CRCI in older patients with cancer. These included serum hemoglobin, brain-derived neurotrophic factor, percent cerebral oxyhemoglobin, functional network connectivity, and individual alpha peak frequency. This review highlights several biomarkers potentially associated with CRCI in older patients with cancer, though consistent and definitive biomarkers remain elusive. Further research is needed to clarify the biological mechanisms underlying CRCI and inform the development of interventions aimed at preventing cognitive decline in this vulnerable population. The identification of validated biomarkers will be critical for advancing personalized nursing and improving clinical outcomes in older adults with cancer. Show less

Alzheimer's disease (AD) is marked by progressive cognitive decline and memory loss. Emerging evidence underscores the role of long non-coding RNAs (lncRNAs), particularly nuclearenriched abundant transcript 1 (NEAT1), in AD pathogenesis. NEAT1, a pivotal lncRNA that regulates diverse cellular processes, shows dysregulated expression in AD and impairs neuronal survival. This review explores NEAT1's molecular mechanisms, biomarker potential, and therapeutic relevance. NEAT1 contributes to AD pathology by acting as a competitive endogenous RNA (ceRNA) that sequesters protective microRNAs, including miR-124 and miR-107, thereby dysregulating downstream targets. It facilitates PINK1 degradation and potentially drives mitochondrial dysfunction and neuronal injury. Elevated NEAT1 levels are associated with amyloid-beta accumulation, tau hyperphosphorylation, and NF-κB-mediated neuroinflammation. Preclinical studies suggest that modulating NEAT1 expression can alleviate AD‑like pathology, making NEAT1 a promising target for intervention. Increased plasma NEAT1 in patients indicates its value as a non-invasive early diagnostic biomarker. NEAT1 regulates multiple AD-related pathways, including IGF1R, TRAF2, BACE1, CREB/BDNF, and Nrf2/NQO1, and interacts with lncRNAs linked to metabolic and neurodegenerative diseases, such as XIST and KCNQ1OT1. By influencing amyloid processing, synaptic function, mitochondrial health, and inflammatory responses, NEAT1 emerges as a central regulator in AD. Targeting NEAT1 offers dual benefits: advancing precision diagnostics and enabling multi-pathway therapeutic approaches. This review underscores NEAT1's significance as both a biomarker and therapeutic target, providing insights for future strategies to mitigate the burden of AD. Show less

The marginal efficiency observed with the existing therapies in Alzheimer's Disease (AD) can be attributed to the timing of the treatment. The beneficiaries of symptomatic or disease-modifying therapy for AD are mild-cognitive-impairment (MCI) or late-stage dementia patients. At this stage, the pathological features are already advanced and irreversible, as the shift in biomarker levels starts in a continuum 15-20 years prior. Early intervention, therefore, is a plausible solution to this issue. Consequently, we selected 3 month-old 5XFAD AD mice as an early intervention model. We administered cannabidiol (CBD) and plasmid brain-derived neurotrophic factor (BDNF) encapsulated in liposome nanoparticles, functionalized with penetratin and mannose for brain-targeting, as a therapy. Neuroinflammation is emerging as a key driver of AD progression by its interaction with amyloid plaques and phosphorylated tau. Therefore, CBD, which is anti-inflammatory and neuroprotective, was used. BDNF, a synaptic modulation and cognitive maintenance agent, is declined and, thus, aggravates pathology and cognition in AD. BDNF expressed from the liposome nanoparticles supplements the reduced BDNF and aids in ameliorating AD pathology. We found four weekly doses of our formulation reduced the amyloid burden by 3.04-fold ( Show less

This chapter explores the diverse range of biomarkers associated with endurance exercise and their relevance for monitoring training adaptation, physiological stress, recovery, and long-term health. Covering cardiovascular (CV), metabolic, hormonal, inflammatory, and neuromodulatory systems, these markers offer valuable insights into how physical activity (PA) affects systemic function. CV parameters such as resting heart rate, heart rate variability, blood pressure (BP), pulse wave velocity, and VO₂max are well-established indicators of fitness and autonomic regulation. Emerging indicators like oxidative stress markers, PGC-1α, and microRNAs provide a window into mitochondrial function and cellular adaptation. Neuromodulators including β-endorphins, endocannabinoids, dopamine, serotonin, and BDNF are discussed in relation to the phenomenon known as the Runner's High, illustrating how endurance exercise can influence mood, perception, and pain sensitivity. The chapter also addresses challenges such as interindividual variability, sampling timing, and practical application. Together, these biomarkers form an integrative framework for evaluating endurance training, optimizing performance, and supporting preventive health strategies across clinical and athletic populations. Show less

Post-traumatic stress disorder (PTSD) causes debilitating nightmares, flashbacks and anxiety stemming from a catastrophic, often life-threatening traumatic event. Originally described in soldiers exposed to the horrors of battle, PTSD is now recognized in civilian victims of assault, natural disasters and mass casualty events. Most people experiencing trauma do not develop PTSD, so understanding neurobiological mechanisms is crucial to predicting risk and developing targeted treatments. There have been many studies seeking to find biomarkers for PTSD, and their results have converged on several brain regions, molecular pathways and neuropsychological functions. In this review, we focus on selected findings about the glucocorticoid receptor (GR), the chaperone protein FKBP51 (FK506 binding protein 51), BDNF (brain-derived neurotrophic factor), fear memory reconsolidation and epigenetic regulation of gene expression in the hypothalamic-pituitary-adrenal (HPA) axis, amygdala and hippocampus. Together, these disparate aspects of brain function provide an emerging model for understanding the etiology and pathophysiology of PTSD. Avoidance of lethal threats is fundamental for survival, and this stringent evolutionary requirement has conserved many components of fear memory storage and behavioural response to danger. PTSD research can therefore rely on non-human animal model systems with better face and construct validity than most other psychiatric disorders. With this advantage, advances in PTSD biomarker identification are likely closer to clinical translation than in other mental illnesses. We attempt to highlight the most promising biomarkers that could be targeted by novel treatments and propose a map for future research work. Show less

To investigate the association between combined vitamin D and N-acetylcysteine (NAC) supplementation and clinical outcomes in patients with generalized anxiety disorder (GAD). This retrospective cohort study included 88 propensity-score-matched patients with GAD from Beidahuang Group Neuropsychiatric Hospital. Based on clinical records, patients were classified into an observation group (vitamin D3 + NAC + usual care) and a control group (usual care only). Anxiety symptoms and cognitive function were assessed using the Beck Anxiety Inventory (BAI), Automatic Thought Questionnaire (ATQ), and Dysfunctional Attitudes Scale (DAS). Serum levels of 25-hydroxyvitamin D [25(OH)D], inflammatory markers [high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6)], oxidative stress parameters [glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD)], and neurochemical markers [brain-derived neurotrophic factor (BDNF), dopamine (DA), Serotonin (5-HT), norepinephrine (NE)] were measured at baseline and week 8. After 8 weeks, both groups showed significant improvements in BAI, ATQ, and DAS scores, with greater reductions in the observation group (all In this retrospective cohort, combined vitamin D and NAC supplementation was associated with significantly greater improvements in anxiety symptoms, cognitive patterns, and relevant metabolic biomarkers in patients with GAD compared to usual care alone, supporting its potential as an adjunctive therapy. Show less

We investigated the association between maternal overactive bladder (OAB) and voiding dysfunction (VD) in their children, and evaluated urinary nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) levels as potential biomarkers for early identification of VD. This prospective cross-sectional study included 196 participants: mothers with OAB (n = 39), their children with VD (n = 36), their children without VD (n = 41), healthy mothers (n = 40), and healthy children of healthy mothers (n = 40). Maternal OAB was diagnosed using the OAB-V8 questionnaire, while VD in children was assessed using the Dysfunctional Voiding Symptom Score (DVSS). Urinary NGF and BDNF levels were measured via ELISA. Receiver operating characteristic (ROC) analyses were performed to assess the diagnostic accuracy of these biomarkers. NGF and BDNF levels were significantly higher in mothers with OAB compared to controls (p < 0.001 for both). Children of OAB mothers with VD demonstrated markedly elevated DVSS scores, NGF, and BDNF levels compared to both healthy children of OAB mothers and children of healthy mothers (all p < 0.001). ROC analysis showed strong diagnostic performance for NGF (AUC = 0.828, cut-off 267.7 pg/ml, 75 % sensitivity, 99 % specificity) and acceptable performance for BDNF (AUC = 0.754, cut-off 3.06 ng/ml, 64 % sensitivity, 93 % specificity). Urinary NGF and BDNF levels were significantly elevated in mothers with OAB and their affected children. NGF demonstrated superior diagnostic accuracy for identifying VD in children, while BDNF may provide complementary value. These findings support the role of neurotrophin-related mechanisms in intergenerational transmission of lower urinary tract dysfunction. Show less

BackgroundPredicting cognitive function across dementia stages remains challenging. Plasma biomarkers and electroencephalogram (EEG) features may provide complementary information, but their combined predictive value requires further study.ObjectiveTo evaluate the feasibility of integrating plasma biomarkers and EEG features to predict cognitive function in dementia and examine their correlations.MethodsFrom September 2023 to October 2024, 75 patients from two medical centers with mild cognitive impairment, mild dementia, or moderate dementia were enrolled. Resting-state 19-channel EEG data yielded 2737 time-frequency and connectivity features. Plasma biomarkers included tau, p-Tau181, Aβ Show less

Pain is common among adults with heart failure (HF), but pain subtypes and associated biomarkers are understudied. The aims were to: 1) characterize chronic pain severity, neuropathic pain quality, locations, and subtypes; and 2) compare pain severity and levels of biomarkers among pain subtypes. An exploratory aim was to correlate levels of biomarkers with pain severity. This pilot descriptive study included cross-sectional data from 60 adults with HF and chronic pain. Pain was evaluated using the PainDETECT questionnaire. Blood biomarkers included interleukin (IL)-10, IL-18, IL-1β, IL-33, IL-6, IL-8, tumor necrosis factor (TNF)-α, brain-derived neurotrophic factor, leptin, adiponectin, and C-reactive protein. Descriptive statistics, Chi-square test of homogeneity, one-way analysis of variance, and Spearman correlation were used for analyses. The mean age was 70.45 (SD 7.92) years. The sample consisted of 63.3% women and 65.0% White race. Participants primarily reported nociceptive pain only (73.3%) with fewer reporting neuropathic pain only (6.7%) and mixed pain (20.0%). Current and 4-week mean pain severity scores were highest in the mixed pain subtype (p both <.05). No biomarkers were significantly different across the pain subtypes, but lower lL-10 (p=.049), and IL-33 (p=.014), were associated with higher pain severity. In this study, chronic pain and its association with underlying biomarkers were characterized. Future research with a larger sample is needed to understand the unique contributions of biomarkers with targeted pain phenotypes. Show less

While mindfulness has demonstrated efficacy in enhancing executive function in non-athletes through improved present-moment awareness and acceptance of current experiences, particularly regarding attention regulation and cognitive control, its neurocognitive mechanisms and the effects and underlying mechanisms of mindfulness-based intervention (MBI) on different executive functioning skills in athletic populations remain poorly understood. The purpose of this randomized controlled trial tackles a novel and important topic by investigating the beneficial effects of 12-week MBI on executive functioning skills in baseball players-a population that faces unique cognitive and physical demands, and the associated neurophysiological and biochemical regulation mechanisms. Thirty-four baseball players were randomly divided into the MBI group (11M/6F) and the control group (11M/6F). Executive functioning skills (N-back task for working memory, Stroop task for inhibitory control, and Switching task for cognitive flexibility) were tested before and after the intervention. Functional near-infrared spectroscopy (fNIRS) was used to record quantified hemodynamic responses in the prefrontal cortex through oxygenated hemoglobin concentration (Oxy-Hb) monitoring during the performance of executive function tasks. Biomarkers of cognitive function, including BDNF, IL-6, TNF-α, and Cortisol, were measured using enzyme-linked immunosorbent assays (ELISA). MBI partially improved all three executive function skills, with increased Oxy-Hb level in L-FPA during the task of working memory, increased Oxy-Hb level in R-VLPFC during the task of inhibitory control, and decreased Oxy-Hb level in R-FPA, M-FPA, and L-DLPFC during the task of cognitive flexibility. Furthermore, MBI increased circulating BDNF level and decreased IL-6 and Cortisol levels. In addition, our correlation analyses showed that improvement in executive function (improved behavioral performances and changes in Oxy-Hb levels) were associated with changes in Cortisol and inflammatory cytokines (TNF-α and IL-6). A 12-week MBI partially improved three components of executive function in baseball players. This enhancement may be attributed to the MBI-induced reductions in Cortisol and inflammatory cytokines (such as TNF-α and IL-6), which altered blood oxygen contents in specific brain regions, thereby promoting executive function. Show less

The role of chemokines in motor abnormalities (MAs) in first-episode psychosis (FEP) is underexplored. Investigating immune biomarker levels in FEP, their association with MAs, and their differences with individuals without FEP may reveal therapeutic targets. Thirty-eight patients and thirty-four controls were included. Primary outcomes assessed group differences in chemokines related immune whole blood biomarkers, including innate (CCL2, CCL3, and CCL11), compensatory (PPARα, CXCL1, and CB2), natural immune chemotaxis biomarkers (CXCL2 and CXCR4), and growth factors (LPAR2, brain-derived neurotrophic factor [BDNF], and vascular endothelial growth factor [VEGF]). Our secondary aim was to examine their association with the total score of five motor scales: the Neurological Evaluation Scale (NES), Simpson Angus Scale (SAS), catatonia symptom of the Comprehensive Assessment of Symptoms and History (CASH), Barnes Akathisia Rating Scale, and Unified Parkinson's Disease Rating Scale (UPDRS). We found significantly higher levels of protein markers (CCL2, VEGF, and CXCL12) and mRNA expression (CXCR4, PPARα, CB2, and LPAR2) in FEP patients compared to the control group. We only observed positive and significant results for CCL2-UPDRS total and CXCR4-SAS associations in post hoc multivariate analyses (β = 0.401, p = 0.036 and β = 0.58, p = 0.001, respectively). Elevated levels of potential neurotoxic (CCL2) and neuroprotective (PPARα and CB2) biomarkers were seen in FEP patients when compared to controls. Moreover, CCL2 levels seem to be directly associated with Parkinsonism in FEP patients, while CXCR4 may be protective against extrapyramidal symptoms. Further research should clarify immune differences between FEP and non-FEP groups, especially in chemotaxis and endocannabinoid pathways. Show less