Plasma Brain-derived Neurotrophic Factor Levels Research Articles

BDNF expression mediates verbal learning and memory in women in a cohort enriched with risk for Alzheimer's disease.

This study examined whether sex differences in verbal learning and memory (VLM) are mediated by plasma brain-derived neurotrophic factor (BDNF) expression. In a sample of n=201 participants (63.81±6.04 years, 66.2% female, 65.7% family history of Alzheimer's disease [AD], 38% apolipoprotein E [APOE] ε4+) from the Wisconsin Registry for Alzheimer's Prevention, VLM was measured using trials 3 through 5 and delayed recall from the Rey Auditory Verbal Learning Test. Plasma BDNF was measured using a Human BDNF Quantikine Immunoassay. Mediation analysis used bootstrapping, and stratified mediation models tested the conditional dependence of APOE ε4 carriage. BDNF partially mediated the sex-VLM relationship (β=-0.07; 95% confidence interval [CI]: -0.18, -0.01). Female APOE ε4 carriers had higher VLM scores (β=-0.53; p=0.03), while female non-carriers had both higher BDNF levels (β=-0.68; p<0.01) and VLM scores (β=-1.06; p<0.01); BDNF was again a significant mediator (β=-0.18; 95% CI: -0.37, -0.05). This study found that circulating BDNF mediates higher verbal memory scores in females-particularly in APOE ε4 non-carriers. Sex differences in verbal learning and memory (VLM) were mediated by plasma brain-derived neurotrophic factor (BDNF) levels.Women exhibited higher VLM scores and plasma BDNF levels compared to men.The protective effect of BDNF in women was attenuated by apolipoprotein E ε4 carriage.Findings suggest sex-specific mechanisms against verbal memory decline in aging.

Differential Effects of Electroconvulsive Therapy on Patients with Schizophrenia Versus Depressive Disorder: Clinical Distinction Between Antipsychotic and Antidepressant Effects of Electroconvulsive Therapy

Objective: Electroconvulsive therapy (ECT) is utilized for treating psychiatric disorders, such as schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BD). We aimed to compare pre- and post-ECT treatment outcomes between patients with SCZ and a combined group of patients with MDD and BD (MDD+BD) to assess the distinction between the antipsychotic and antidepressant effects of ECT. Methods: ECT was administered to patients with SCZ (n = 17) and those with MDD+BD (n = 7). Symptoms were evaluated using the brief psychiatric rating scale (BPRS), clinical global impression scale (CGI), and global assessment of functioning (GAF). Plasma brain-derived neurotrophic factor (BDNF) levels were also measured. Results: The BPRS, CGI, and GAF scores significantly differed after ECT compared with those before ECT in each patient group. However, no significant differences were observed between the groups for each disorder. No significant differences were observed in plasma BDNF levels between the groups at baseline and during ECT. At baseline, only depression scores were more favorable in the SCZ group, whereas positive symptoms and disorganization scores were higher in the MDD+BD group. During treatment, positive symptoms, activation, and disorganization items were significantly more favorable in the MDD+BD group compared with the SCZ group. Total BPRS scores were not associated with plasma BDNF levels; however, rating scores of the several items related to activation, resistance, and disorganization were positively correlated with BDNF levels. Conclusion: ECT effects on several clinical outcomes in the MDD+BD group were associated with plasma BDNF levels. These findings suggest that ECT may be more effective for treating MDD than SCZ.

Differences in Plasma BDNF Levels Between Chronic Primary Musculoskeletal Pain, Fibromyalgia Syndrome, and Asymptomatic Subjects: A Cross-Sectional Study.

This cross-sectional study compared plasma brain-derived neurotrophic factor (BDNF) levels among chronic primary musculoskeletal pain patients, chronic widespread pain patients, and asymptomatic controls. The study included 126 participants aged 18-65, divided into three groups of 42 each. Pain intensity was assessed using a Numeric Rating Scale (NRS), and plasma BDNF levels were measured via ELISA. Differences between groups were evaluated using ANOVA with 2000 bootstrap resamples and a bias-corrected and accelerated method. Results showed significantly higher plasma BDNF levels in chronic widespread pain patients (mean difference [MD] = 0.44; 95% CI = 0.28, 0.62; p < .001) compared to controls, and higher than in chronic primary musculoskeletal pain patients (MD = 0.83; 95% CI = 0.64, 1.02; p < .001). Chronic primary musculoskeletal pain patients had lower plasma BDNF levels compared to controls (MD = -0.39; 95% CI = -0.54, -0.24; p < .001). No significant correlations were observed between plasma BDNF levels and clinical variables. These findings suggest the potential of BDNF as a biomarker to differentiate chronic primary pain conditions.

Brain-Derived Neurotrophic Factor (BDNF) as a Potential Biomarker in Brain Glioma: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluates peripheral and CNS BDNF levels in glioma patients. Following PRISMA guidelines, we systematically searched databases for studies measuring BDNF in glioma patients and controls. After screening and data extraction, we conducted quality assessment, meta-analysis, and meta-regression. Eight studies were included. Meta-analysis showed significantly reduced plasma BDNF levels in glioma patients versus controls (SMD: -1.0026; 95% CI: [-1.5284, -0.4769], p = 0.0002). High-grade gliomas had lower plasma BDNF (p = 0.0288). Tissue BDNF levels were higher in glioma patients (SMD: 1.9513; 95% CI: [0.7365, 3.1661], p = 0.0016) and correlated with tumor grade (p = 0.0122). Plasma BDNF levels negatively correlated with patient age (p = 0.0244) and positively with female percentage (p = 0.0007). BDNF is a promising biomarker in glioma, showing significant changes in plasma and tissue levels correlating with tumor grade, patient age, and gender.

Effect of systemic ozone therapy added to pharmacological treatment on brain-derived neurotrophic factor (BDNF) and cognitive status in post-COVID patients

BACKGROUND: Treatment is required for post-COVID cognitive impairment associated with functional limitations, reduced work capacity, and significant deterioration in quality of life. Pharmacological treatment is ineffective. In this context, physical therapy, especially systemic ozone therapy with potential neuroprotective effects, appears promising. AIM: The aim of the study was to evaluate the effect of systemic ozone therapy added to pharmacological treatment on plasma brain-derived neurotrophic factor (BDNF) levels and cognitive status in patients with post-COVID cognitive impairment. MATERIALS AND METHODS: A total of 140 patients aged 18-45 years with post-COVID asthenic syndrome were evaluated and treated. They were randomized into two groups: an experimental group with 70 subjects who received systemic ozone therapy in addition to pharmacological treatment and the comparator group with 70 subjects who received pharmacological treatment only. Pre- and post-treatment outcomes were assessed using plasma BDNF levels and the Montreal Cognitive Assessment (MoCa) score. RESULTS: Statistically significant differences in BDNF levels (р=0.034) and MoCa scores (р=0.002) were found between the compared groups at the end of therapy (day 30). In our study, adding systemic ozone therapy to pharmacological treatment in patients with post-COVID cognitive impairment normalized BDNF levels and completely improved clinical manifestations of cognitive impairment in 95% of subjects. CONCLUSION: Therefore, systemic ozone therapy can be considered as one of the effective and pathogenetically proven strategies for comprehensive treatment of patients with post-COVID cognitive impairment in the outpatient setting.

Exploring the impact of childhood maltreatment on epigenetic and brain-derived neurotrophic factor changes in bipolar disorder and healthy control.

Childhood maltreatment may be linked to epigenetics and brain-derived neurotrophic factor (BDNF) changes, which are mechanisms altered in several psychiatric conditions, including bipolar disorder (BD). However, the specific mechanisms connecting childhood maltreatment to the pathophysiology of BD remain unclear. The present study aims to examine the effects of childhood maltreatment on epigenetic and neurotrophic outcomes in BD patients and health controls. History of childhood maltreatment was obtained using the Childhood Trauma Questionnaire (CTQ) from 36 BD outpatients and 46 healthy subjects. DNA methyltransferase (DNMT) activity, HMTH3K9 activity, histone 3 lysine 9 tri-methylation (H3K9me3) levels, histone deacetylase (HDAC)1 levels, HDAC2 levels, histone 3 lysine 14 acetylation (H3K14ac) levels, and mRNA of BDNF were evaluated in peripheral blood mononuclear cells. Plasma BDNF levels were also measured. Total scores of CTQ, as well as the subscale scores of emotional abuse, sexual abuse, and emotional neglect, were predictive of changes in DNMT and HMTh3k9 activity, H3K9m3 levels, BDNF mRNA expression, and BDNF levels. These findings were observed in all our samples and, in some cases, among BD patients. Emotional abuse was the main childhood maltreatment subtype associated with epigenetic alterations in BD. Our results elucidate some mechanisms by which childhood maltreatment can alter epigenetic and neurotrophic markers. Especially in BD subjects, our results suggest childhood maltreatment per se is not a direct cause for epigenetic alterations. In another way, we suppose that the effect of childhood maltreatment could be cumulative and interact with other factors associated with the pathophysiology of BD.

Plasma Brain-Derived Neurotrophic Factor (BDNF) Levels and BDNF Promoters' DNA Methylation in Workers Exposed to Occupational Stress and Suffering from Psychiatric Disorders.

Decreased plasma BDNF (pBDNF) levels have been proposed as a biomarker in the illness phases of mood disorders. This cross-sectional study aimed to evaluate the pBDNF and BDNF promoters' DNA methylation levels in workers exposed to occupational stress and suffering from work-related stress disorders. the pBDNF and BDNF exon I and IV promoters' methylation levels were measured by specific immunoassays and methylation-sensitive high-resolution melting (MS-HRM) in 62 patients with adjustment disorders (AD), 79 patients with major depressive disorder (MDD) and 44 healthy controls. Occupational stress was evaluated in the patients and controls using the Job Content Questionnaire (JCQ). the pBDNF levels were significantly higher in the MDD (p < 0.001) and AD (p < 0.0001) patients than in the controls. The MDD patients showed significantly lower pBDNF levels than the AD ones (p = 0.01). The BDNF exon I and IV promoters' methylation levels were significantly higher in the MDD patients than in the AD ones (exon I promoter: p = 0.0001, exon IV promoter: p < 0.0001) and controls (exon I promoter: p = 0.0001, exon IV promoter: p < 0.0001). In the patients, but not in the controls, the BDNF promoters' methylation levels showed significant negative correlations with occupational stress. BDNF could play a key role in the pathophysiology of stress-related disorders and the peripheral elevation of it observed in patients exposed to occupational stress could suggest a protective mechanism for neurons from stress-mediated damage. The elevation of the pBDNF levels, even in MDD, may characterize a "reactive" subtype of depressive episode, while the significant elevation of the BDNF promoters' methylation levels in depressed patients could indicate a predisposition to more severe illness under stress. Further research is needed, focusing on biomarkers for stress-related disorders as a potential tool for the diagnosis and prevention of occupational diseases.

From a solitary blood-derived biomarker to combined biomarkers of sarcopenia: Experiences from the Korean Frailty and Aging Cohort Study.

Sarcopenia is recognized as a complex and multifactorial disorder that includes nutritional deficiency, inactivity, proinflammatory status, hormonal changes, neurological degeneration, and metabolic disturbances. Its' pathogenesis is not fully understood. Therefore, identifying specific biomarkers of sarcopenia will help us understand its pathophysiology. The most frequently reported blood-derived biomarkers of sarcopenia are growth factors, neuromuscular junctions, endocrine systems, mitochondrial dysfunction, inflammation-mediated and redox processes, muscle protein turnover, blood metabolomics, and behavior-mediated biomarkers. Here, we address the implications of sarcopenia biomarkers based on our research experience with KFACS cohort data. It includes free testosterone, myostatin, fibroblast growth factor 21 (FGF-21), growth differentiation factor 15 (GDF-15), procollagen type III N-terminal peptide (P3NP), creatinine-based biomarkers, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), brain-derived neurotrophic factor (BDNF), metabolites (proline, alanine, tryptophan), and multi-biomarker risk score. We attempted to explain the paradoxical findings of myostatin and FGF-21 levels in relation to sarcopenia. GDF-15 levels were associated with sarcopenia prevalence but not its incidence. Plasma P3NP and BDNF levels may be biomarkers of muscle quality rather than quantity. Lower erythrocyte EPA and DHA levels were associated with slow gait speed, and erythrocyte EPA levels were associated with low handgrip strength. We developed a multi-biomarker risk score for sarcopenia and found that its accuracy in diagnosing sarcopenia was higher than that of any single biomarker.

Effects of chronic stress on rat heart function following regional ischemia: a sex-dependent investigation.

Chronic psychological stress is a recognized, yet understudied risk factor for heart disease, with potential sex-specific effects. We investigated whether chronic stress triggers sex-dependent cardiac dysfunction in isolated Wistar rat hearts subjected to ischemia-reperfusion injury. The experimental cohort underwent 1 h of daily restraint stress for 4 wk versus matched controls, followed by euthanasia (sodium pentobarbital) and heart excision for ex vivo perfusion. Blood analysis revealed sex-specific alterations in stress hormones and inflammatory markers. When compared with controls, chronic restraint stress (CRS) males displayed decreased plasma brain-derived neurotrophic factor (BDNF) levels (P < 0.05), whereas CRS females exhibited elevated plasma adrenocorticotropic hormone (ACTH) (P < 0.01) and reduced corticosterone (P < 0.001) alongside lower serum estradiol (P < 0.001) and estradiol/progesterone ratio (P < 0.01). Of note, CRS females showed increased serum cardiac troponin T (P < 0.05) and tumor necrosis factor-α (TNF-α) (P < 0.01) with suppressed interleukin (IL)-1α, IL-1β, IL-6, and IL-10 levels (P < 0.05) when compared with controls. Ex vivo Langendorff perfusions revealed that CRS female hearts displayed impaired postischemic functional recovery for baseline stroke volume (SV, P < 0.01), work performance (P < 0.05), aortic output (AO, P < 0.05), coronary flow (CF, P < 0.01), and overall cardiac output (CO, P < 0.01) when compared with matched controls and CRS males (P < 0.05). Our findings reveal intriguing sex-specific responses at both the systemic and functional levels in stressed hearts. Here, the dysregulation of stress hormones, proinflammatory state, and potential underlying cardiomyopathy in females following the stress protocol renders them more prone to damage following myocardial ischemia. This study emphasizes the importance of incorporating sex as a biological variable in cardiac research focusing on stress-related cardiomyopathy.NEW & NOTEWORTHY Although chronic psychological stress is a risk factor for cardiovascular diseases, the underlying mechanisms remain poorly understood. This study revealed that chronic restraint stress resulted in systemic changes (dysregulated stress hormones, proinflammatory state) and potential cardiomyopathy in females versus controls and their male counterparts. The stressed female hearts also displayed reduced functional recovery following ex vivo ischemia-reperfusion. This highlights the importance of incorporating sex as a biological variable in cardiac research.

Assessment of BDNF and sialic acid levels in children with ADHD: Relation of chronotypes.

Evaluation of the biomarkers and their relations with sleep in attention deficit hyperactivity disorder (ADHD) is important for understanding the impairments in cognitive functioning. In this study, we aimed to investigate the brain-derived neurotrophic factor (BDNF) and sialic acid (Sia) levels, and their possible relations with chronotypes in ADHD. The study included 100 drug-naive children with ADHD and 74 healthy children as controls. Conners' Parent Rating Scale-Revised (CPRS-R) scores were used for the severity assessment. Morningness Eveningness Questionnaire (MEQ) was used to determine the chronotypes of participants. ELISA kits were used for the assessment of BDNF and Sia plasma levels. Levels of BDNF and Sia were found to be statistically significantly higher in the ADHD group compared to healthy children (p < 0.001, p < 0.001, respectively). BDNF and Sia levels were found to be higher in the ADHD group with eveningness chronotype (p = 0.045, p = 0.038). The binary logistic regression model was statistically significant (p = 0.033), higher BDNF and Sia levels were assessed as predictive factors for the diagnosis of ADHD. Also, eveningness chronotype was found as a predictive factor of BDNF and Sia levels in ADHD. The results indicate that BDNF and Sia levels, which are related to cognitive functions and sleep, increase with the age of ADHD. Eveningness chronotype, connected with the severity of ADHD, is related to BDNF and Sia levels. There is a need for further studies to confirm these results.

Investigating Neuroplasticity Changes Reflected by BDNF Levels in Astrocyte-Derived Extracellular Vesicles in Patients with Depression.

To investigate the neuroplasticity hypothesis of depression by measuring brain-derived neurotrophic factor (BDNF) levels in plasma astrocyte-derived extracellular vesicles (ADEVs) and to evaluate their potential as biomarkers for depression compared with plasma BDNF levels. Thirty-five patients with major depressive disorder (MDD) and 35 matched healthy controls (HCs) were enrolled. Plasma ADEVs were isolated using a combination of ultracentrifugation and immunoaffinity capture. Isolated ADEVs were validated using transmission electron microscopy, nanoparticle tracking analysis, and Western blotting. BDNF levels were quantified in both ADEVs and plasma. ALG-2-interacting protein X (Alix) and cluster of differentiation 81 (CD81) levels, two established extracellular vesicle markers, were measured in ADEVs. After false discovery rate correction, patients with MDD exhibited higher CD81 levels (P FDR = 0.040) and lower BDNF levels (P FDR = 0.043) in ADEVs than HCs at baseline. BDNF levels in ADEVs normalized to CD81 (P FDR = 0.002) and Alix (P FDR = 0.040) remained consistent with this finding. Following four weeks of selective serotonin reuptake inhibitor treatment (n=10), CD81 levels in ADEVs decreased (P FDR = 0.046), while BDNF levels normalized to CD81 increased (P FDR = 0.022). BDNF levels in ADEVs were more stable than in plasma. Exploratory analysis revealed no correlation between BDNF levels in ADEVs and plasma (ρ=0.117, P = 0.334). This study provides human in vivo evidence supporting the neuroplasticity hypothesis of depression by demonstrating altered BDNF levels in ADEVs. ADEVs may be more suitable for developing biomarkers of depression than plasma-derived biomarkers.

P18: BDNF levels and affective disorders as a marker of vulnerability to developing cognitive impairment in the Chilean adult population

Summary: Disorders related to progressive cognitive decline constituting an important cause of global death and disability-adjusted life years because conditions are also associated to impairment of several brain functions, psychological and behavioral changes, regardless of economic status. Brain-derived neurotrophic factor (BDNF) is a neurotrophin highly relevant in memory, learning and neuroplasticity processes in adults. The amount of plasma BDNF has been considered to partly reflect its secretion in the brain. Its deficiency is associated with affective disorders and neurodegenerative pathologies such as Alzheimer disease and Parkinson’sdisease.The aim of this study was to identify quantifiable biomarkers (serum levels of BDNF) and clinical marker (state of depression and anxiety) that allow early detection of cognitive impairment risk. We made an analytic and transversal study with a representative sample (n:307) of the population over 50 years old in the south of Chile (X region). We determine the cognitive condition of the population by applying cognitive functionality tests, such as the minimental status examination (MMSE) test and identify demographic and psychosocial characteristics that constitute impairment cognitive risk. Subsequently, we determined depression status (scale of Yesavage) and anxiety status (Beck inventory), and finally we made a quantitative determination of human BDNF at the blood level using ELISA technique.Our results revealed that 26.7% of the participants exhibited some degree of cognitive impairment, being higher in women (55.7%) with average age of 70,7. A 18,2% of subjects manifested indicators of depression and 33,2% have a very hight level of anxiety. The correlation analysis revealed a significant positive correlation between MMSE test (p &lt; 0.001) and both BDNF plasma levels (p &lt; 0.001) and education level (p &lt; 0.001) scores. The results additionally indicated a negative correlation between cognitive functions and age range/anxiety state, suggesting low age level/hight level of anxiety in subjects with more pronounced cognitive decline (p &lt; 0.001),. In consistent, the results of our study point towards decreases plasma BDNF levels and hight levels of anxiety in cognitive impairment subjects compared with cognitive normal subjects, which may be due to the early and middle stages of neurodegeneration process.

Optimizing esketamine administration for postoperative depression: a comprehensive study on laparoscopic bariatric surgery patients

BackgroundPrevious studies have reported conflicting findings regarding the efficacy of esketamine in managing postoperative depression. While the positive effects of subanesthetic doses esketamine have been observed in treatment-resistant depression, the response to this medication in patients experiencing depression following surgery has not been consistent. Building upon the known impact of anesthesia on brain function, we have formulated a hypothesis suggesting that the timing of esketamine administration in relation to anesthesia may significantly affect its efficacy in managing postoperative depression. The aim of this study was to investigate the effect of esketamine administered at different time points before and after anesthesia.MethodsOur randomized, double-blind, controlled study involved 120 patients undergoing laparoscopic bariatric surgery, randomly divided into three groups. Group Post- ESK received an intravenous injection of esketamine at a dose of 0.2 mg/kg after anesthesia induction. Group Pre- ESK received the same esketamine dosage 2 h prior to anesthesia induction. Group Placebo served as the control group and received a 0.9% saline solution after induction. The primary outcome measures of the study were depression scores as measured by Patient Health Questionnaire-9 (PHQ-9) and plasma brain-derived neurotrophic factor (BDNF) levels.ResultsOn the first postoperative day, the PHQ-9 scores, incidence and severity of postoperative depression in the Pre-ESK group were significantly lower than those in the Post-ESK and placebo groups (P < 0.05). Additionally, plasma BDNF levels in the Pre-ESK group were significantly higher than those in the Post-ESK and placebo groups (P < 0.05). Notably, there was a negative correlation between PHQ-9 scores and plasma BDNF levels.ConclusionsOur study supports the potential for subanesthetic dose esketamine to alleviate postoperative depression symptoms following laparoscopic bariatric surgery, and anesthetic drugs have a significant effect on its efficacy. The use of subanesthetic dose esketamine after anesthesia does not improve postoperative depression symptoms in patients undergoing laparoscopic bariatric surgery, while the use of sub-anesthetic dose esketamine before anesthesia can improve postoperative depression symptoms.

Effects of 9 Weeks of High- or Moderate-Intensity Training on Cardiorespiratory Fitness, Inhibitory Control, and Plasma Brain-Derived Neurotrophic Factor in Danish Adolescents-A Randomized Controlled Trial.

The primary aims of this study were to examine the effects of 9 weeks of aerobic training, comprising three 30-min sessions per week, on V̇O2max, inhibitory control, and plasma brain-derived neurotrophic factor (BDNF) levels among adolescents aged 16-19 years. One hundred twenty-one untrained or recreationally active adolescents from a Danish high school were enrolled in the study, with 58 females (17.8 ± 0.8 years) and 27 males (18.0 ± 0.9 years) completing it. Participants were randomly divided into three groups performing aerobic training at either moderate-intensity (MIT: 60%-70% heart rate reserve [HRR]) or high-intensity (HIT: 80%-100% HRR) or a passive control group (CON) continuing their habitual lifestyle. Both the training groups exercised for 3×30 min per week for 9 weeks using a combination of cycling and running. Before and after the intervention period maximal oxygen uptake (V̇O2max) and the primary outcomes (inhibitory control measured by a modified flanker task, and resting plasma levels of BDNF) were evaluated. After the intervention period, the HIT group demonstrated a larger increase in V̇O2max compared to both the CON and MIT groups, while no significant effects were observed on inhibitory control or plasma BDNF levels in any training group. However, compared to the CON group, the HIT group exhibited a tendency for greater improvement in the flanker interference score (accuracy), attributable to enhanced accuracy on the incongruent stimuli from pre to post. Aerobic training in adolescents increased cardiorespiratory fitness in an intensity-dependent manner, but no clear effects were observed on neither inhibitory control nor resting plasma BDNF levels. ClinicalTrials.gov: NCT02075944.

Investigating the role of TGF-β and BDNF in cancer-related depression: a primary cross-sectional study.

Cancer-related depression is a well-documented condition that significantly impacts long-term quality of life. Brain-derived neurotrophic factor (BDNF), a neurotrophin essential for neurogenesis and neuronal plasticity, has been implicated in various neuropsychological disorders including depression associated with cancer. Cytokines, on the other hand, play a crucial role in regulating depression, potentially by influencing BDNF expression. Transforming growth factor-β (TGF-β), a key immune regulator within the tumor microenvironment, has been found to elevate BDNF levels, establishing a link between peripheral immune responses and depression. The study aims to investigate the correlation of TGF-β and BDNF in cancer-related depression. This study involved a cohort of 153 gynecological patients, including 61 patients with gynecological cancer and 92 patients without cancer. Depression levels were assessed using the subscale of Hospital Anxiety and Depression Scale (HADS-D), and TGF-β and BDNF plasma levels were measured using enzyme-linked immunosorbent assay (ELISA). The study revealed elevated plasma TGF-β levels in patients with cancer (32.24 ± 22.93 ng/ml) compared to those without cancer (25.24 ± 19.72 ng/ml) (P = 0.046). Additionally, reduced levels of BDNF were observed in patients presenting depression symptoms (44.96 ± 41.06 pg/ml) compared to those without depression (133.5 ± 176.7 pg/ml) (P = 0.036). Importantly, a significant correlation between TGF-β and BDNF was found in patients without cancer but with depression (correlation coefficient = 0.893, **P < 0.01). Interestingly, cancer appeared to influence the association between TGF-β and BDNF in patients with depression, as evidenced by a significant difference in the correlation of TGF-β and BDNF between cancer and non-cancer groups (P = 0.041). These findings underscore the active involvement of TGF-β and BDNF crosstalk in the context of cancer-related depression.

Relationship between plasma brain-derived neurotrophic factor levels and neurological disorders: An investigation using Mendelian randomisation

BackgroundAltered brain-derived neurotrophic factor (BDNF) concentrations have been detected in the central nervous system tissues and peripheral blood. These alterations are associated with a series of neurological disorders. ObjectiveTo investigate the potential causal relationships between genetically determined plasma BDNF levels and various neurological diseases using a two-sample Mendelian randomisation study. MethodsWe selected single nucleotide polymorphisms strongly related to plasma BDNF levels as instrumental variables. Within the Mendelian randomisation framework, we used summary-level statistics for exposure (plasma BDNF levels) and outcomes (neurological disorders). ResultsWe observed suggestive evidence of a relation between higher plasma BDNF levels and less risk of nontraumatic intracranial haemorrhage (nITH) (odds ratio [OR] = 0.861, 95 % confidence interval [CI]: 0.774–0.958, P = 0.006, PFDR = 0.078), epilepsy (OR = 0.927, 95 % CI: 0.880–0.976, P = 0.004, PFDR = 0.078), focal epilepsy (OR = 0.928, 95 % CI: 0.874–0.986, P = 0.016, PFDR = 0.139), and non-lesional focal epilepsy (OR = 0.981, 95 % CI: 0.964–0.999, P = 0.041, PFDR = 0.267). Combined with the UK Biobank dataset, the association of plasma BDNF levels with nITH remained significant (OR = 0.88, 95 % CI: 0.81–0.96, P < 0.01). The combined analysis of three consortium datasets demonstrated a considerable impact of plasma BDNF on epilepsy (OR = 0.94, 95 % CI: 0.90–0.98, P < 0.01) and a suggestive impact on focal epilepsy (OR = 0.94, 95 % CI: 0.89–0.99, P = 0.02). However, there was no apparent correlation between plasma BDNF levels and other neurological disorders or related subtypes. ConclusionsOur study supports a possible causal relationship between elevated plasma BDNF levels and a reduced risk of nITH, epilepsy, and focal epilepsy.

Expression Patterns of miRNAs in Egyptian Children with ADHD: Clinical Study with Correlation Analysis

ADHD has huge knowledge gaps concerning its etiology. MicroRNAs (miRNAs) provide promising diagnostic biomarkers of human pathophysiology and may be a novel therapeutic option. The aim was to investigate the levels of miR-34c-3p, miR-155, miR-138-1, miR-296-5p, and plasma brain-derived neurotrophic factor (BDNF) in a group of children with ADHD compared to neurotypicals and to explore correlations between these measures and some clinical data. The participants were children with ADHD in Group I (N = 41; age: 8.2 ± 2) and neurotypical ones in Group II (N = 40; age: 8.6 ± 2.5). Group I was subjected to clinical examination, the Stanford Binet intelligence scale-5, the preschool language scale, and Conner’s parent rating scale-R. Measuring the expression levels of the miRNAs was performed by qRT-PCR for all participants. The BDNF level was measured by ELISA. The lowest scores on the IQ subtest were knowledge and working memory. No discrepancies were noticed between the receptive and expressive language ages. The highest scores on the Conner’s scale were those for cognitive problems. Participants with ADHD exhibited higher plasma BDNF levels compared to controls (p = 0.0003). Expression patterns of only miR-34c-3p and miR-138-1 were downregulated with significant statistical differences (p˂0.01). However, expression levels of miR-296-5p showed negative correlation with the total scores of IQ (p = 0.03). MiR-34c-3p, miR-138-1, while BDNF showed good diagnostic potential. The downregulated levels of miR-34c-3p and miR-138-1, together with high BDNF levels, are suggested to be involved in the etiology of ADHD in Egyptian children. Gender differences influenced the expression patterns of miRNAs only in children with ADHD.

Brain neurotrophic factor BDNF: new data, functions and questions

The brain-derived neurotrophic factor (BDNF) is a key modulator of neurogenesis, synaptogenesis, neuroregeneration, and cell differentiation in the nervous system. Impaired BDNF functioning is a characteristic of various neurological diseases, such as Alzheimer’s disease, multiple sclerosis, and depressive disorders. There is recent evidence that patients with COVID-19 have reduced BDNF levels in the blood plasma. Furthermore, exogenous BDNF and its mimetics have demonstrated therapeutic potential.&#x0D; In this review, we systematized data of the BDNF gene structure, epigenetic and microRNA-mediated regulation of its expression, transcriptional variants of BDNF, and the effects of BDNF on neuronal and oligodendroglial differentiation. Further, we point out the gaps in the current knowledge about BDNF and propose experiments that can expand such knowledge and the range of possibilities for using BDNF in biomedicine. These include determining the expression pattern of all BDNF gene transcripts at different stages of differentiation and in different cell subpopulations and studying the role of receptor-independent BDNF signaling, circadian fluctuations in BDNF levels, and their role in physiological and pathophysiological conditions. Finally, for translational medicine, evaluating the effect of BDNF mimetics (including those immobilized on three-dimensional scaffolds for tissue engineering) on neuronal and oligodendroglial differentiation of pluripotent and polypotent cells and identifying molecular regulators of BDNF transcription, including small molecules and microRNAs capable of regulating BDNF gene expression, are crucial.

An analysis of the relationship of "the Mozart effect" with BDNF levels in anatomy education.

In 1993, an increase was observed in the spatial IQ scores of the volunteers who listened to Mozart's sonata K448 for 10 min, and this phenomenon entered the literature as the "Mozart effect." Other studies have shown that this effect is particularly evident in spatial skill tests. A large body of research has provided evidence that spatial ability is associated with success in learning anatomy. In this study, Kastamonu University Faculty of Medicine students were divided into two groups during 16-h practical training spanning 30 days. While one of the groups listened to Mozart's K448 sonata as the background music in all lessons, the control group attended the lessons in their standard form. At the end of each lesson, all students solved a modified mental rotation test including questions involving anatomical structures. Before starting the study, after the first laboratory class, on the 15th and 30th day of the study, blood samples were taken from the participants, and plasma brain-derived neurotrophic factor (BDNF) levels were determined. The effect of time on mental rotation score and plasma BDNF level was significant (p < 0.001 for both). The effect of group was also significant (p < 0.001 for both). Pairwise comparisons showed significance in the fifth, sixth, seventh, and eighth mental rotation test (p < 0.001, p = 0.041, p < 0.001, p < 0.001, respectively) and in the third (Day 15) and fourth (Day 30) BDNF measurement (p < 0.001 for both). Our findings may indicate that specific background music may be useful for anatomy teaching.

How BDNF affects working memory in acute sleep deprivation: The mediating role of spontaneous brain activity

The brain-derived neurotrophic factor (BDNF) mediates the plasticity associated with memory processing, and compensatorily increases after acute sleep deprivation (SD). However, whether the altered spontaneous brain activity mediates the association between BDNF and working memory in SD remains unknown. Here, we aimed to probe the mediating role of the spontaneous brain activity between plasma BDNF and WM function in SD. A total of 30 healthy subjects with regular sleep were enrolled in this study. Resting-sate functional magnetic resonance imaging (fMRI) scans and the peripheral blood were collected before and after 24 h SD. All participants also received n-back task assessing working memory (WM) performance. The amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (fALFF) were calculated to reflect the intensity of regional spontaneous brain activity. Plasma BDNF was measured by sandwich ELISA. Our results revealed a significant decline in WM and increase in plasma BDNF level after SD, and negative association between the changed WM performance and plasma BDNF level. Specially, the ALFF of the left inferior parietal cortex and right inferior frontal cortex, and fALFF of the left anterior cingulate and medial prefrontal cortex and left posterior opercular cortex regulated the association between the BDNF and one-back reaction time respectively. Our results suggest that the association between BDNF and working memory may be mediated through regional spontaneous brain activity involving in the cerebral cortex, which may provide new sight into the interaction between neurotrophic factors and cognition, and potential targets for noninvasive brain stimulation on WM decline after acute SD.