Brain-derived Neurotrophic Factor Levels Research Articles

Role of Cardiovascular Risk in Associations of Brain-Derived Neurotrophic Factor with Longitudinal Brain and Cognitive Trajectories in Older Adults

ABSTRACT Background Higher levels of brain-derived neurotrophic factor (BDNF) have been associated with better neurocognitive outcomes. BDNF is present in cardiovascular tissue, and some evidence suggests it may benefit cardiovascular function. The current study assessed whether there is a mediating and/or moderating role of cardiovascular health in the relationship between BDNF and brain and cognitive outcomes. Method We examined longitudinal data from 397 older adults (aged 54–89;164 females, 233 males) enrolled in the Alzheimer’s Disease Neuroimaging Initiative with available plasma BDNF, medical, neuroimaging, and cognitive assessments. We used path analysis and linear regression to estimate the mediating and moderating roles of two measures of cardiovascular health, the Framingham Risk Score (FRS) and pulse pressure, in the relationships between BDNF and longitudinal changes in brain structure (white matter hyperintensity volume, hippocampal volume, and primary visual cortex volume) and cognitive function (executive function, episodic memory, and language). Results There was no significant association of plasma BDNF with FRS or pulse pressure (ps > 0.31), precluding mediation. There were no robust associations between BDNF and longitudinal change in any brain structural or cognitive measures (ps > .12). Higher FRS was significantly associated with greater increases in WMH volume (ps < .01). FRS and pulse pressure were not associated with any other brain structural or cognitive outcomes (ps > .07). Conclusion These results suggest that cardiovascular health may not play an important role in the influence of BDNF on neurocognitive health in older adults.

BDNF and Cerebellar Ataxia.

Brain-derived neurotrophic factor (BDNF) has been proposed as a treatment for neurodegeneration, including diseases of the cerebellum, where BDNF levels or those of its main receptor, TrkB, are often diminished relative to controls, thereby serving as replacement therapy. Experimental evidence indicates that BDNF signaling countered cerebellar degeneration, sensorimotor deficits, or both, in transgenic ATXN1 mice mutated for ataxin-1, Cacna1a knock-in mice mutated for ataxin-6, mice injected with lentivectors encoding RNA sequences against human FXN into the cerebellar cortex, Kcnj6Wv (Weaver) mutant mice with granule cell degeneration, and rats with olivocerebellar transaction, similar to a BDNF-overexpressing transgenic line interbred with Cacng2stg mutant mice. In this regard, this study discusses whether BDNF is effective in cerebellar pathologies where BDNF levels are normal and whether it is effective in cases with combined cerebellar and basal ganglia damage.

Jianghua Kucha black tea containing theacrine attenuates depression-like behavior in CUMS mice by regulating gut microbiota-brain neurochemicals and cytokines

Theacrine and theaflavins are known for their potential to mitigate depression and cognitive impairment. Jianghua Kucha black tea (JH) contains both compounds, yet its antidepressant properties are seldom documented. This study evaluated the effects of JH on depression in chronic unpredictable mild stress (CUMS) mice and explored the underlying mechanisms through integrative analyses of gut microbiota and fecal metabolomics. JH was found to significantly alleviate CUMS-induced depression-like behavior by improving body weight, food intake, 1% sucrose preference, immobility time, and numbers of crossings and standings compared to Zhuyeqi black tea (ZYQ), which contains theaflavins. JH notably altered the gut microbiota composition, enriching genera such as Turicibacter, Faecalibaculum, Akkermansia, and Desulfovibrio, while inhibiting genera norank_f__Muribaculaceae and Lactobacillus. Additionally, JH modified the fecal metabolite profile, characterized by increased levels of several secondary bile acids (BAs) and decreased levels of several purine intermediate metabolites. Furthermore, JH upregulated levels of monoamine neurotransmitters (5-HT and DA) and brain-derived neurotrophic factor (BDNF), while downregulating pro-inflammatory cytokines IL-6 and TNF-α in brain tissue. These findings suggested that JH could mitigate CUMS-induced depression-like behavior, potentially by modulating gut microbiota composition and function, as well as brain neurochemicals and cytokines.

Effects of variation in exercise training load on cognitive performances and neurotrophic biomarkers in patients with coronary artery disease.

This study compared the effects of linear (LP) and nonlinear (NLP) training periodization on cognitive functions, neurotrophic biomarkers [plasma brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1)], and cathepsin-B in patients with coronary artery disease (CAD). Forty-four patients with CAD reported to our laboratory on two occasions to undergo testing procedures before and after training sessions, and were then blindly randomized to NLP or LP for 36 training sessions. Visit 1 included blood samples and a maximal cardiopulmonary exercise testing to get maximal oxygen uptake (V̇o2peak). Visit 2 included cognitive functions assessment. Thirty-nine patients completed the study (LP: n = 20, NLP: n = 19), with no observed changes in cognitive performances after the training intervention in either group. IGF-1 concentration decreased in both groups (time-effect: P < 0.001), whereas BDNF concentration increased (time-effect: P < 0.05) without group interaction, and cathepsin-B did not change after the intervention. Associations were found between ΔV̇o2peak and ΔBDNF (R2 = 0.18, P = 0.04), and ΔIGF-1 and Δshort-term/working memory (R2 = 0.17, P = 0.01) in the pooled sample, with ΔIGF-1 and ΔBDNF accounting for 10% of the variance in Δshort-term/working memory. In the LP group, associations were found between ΔV̇o2peak and ΔBDNF (R2 = 0.45, P = 0.02), ΔBDNF and Δshort-term/working memory (R2 = 0.62, P = 0.004), ΔIGF-1 and Δshort-term/working memory (R2 = 0.31, P = 0.01), and ΔIGF-1 and Δexecutive function (R2 = 0.22, P = 0.04). This study indicates that linear and nonlinear training periodization led to an increase in BDNF, and a decrease in IGF-1, without change in cognitive function in individuals with stable CAD.NEW & NOTEWORTHY We used a novel and supervised iso-energetic training, integrating both moderate- and high-intensity aerobic exercises. Our findings indicate that greater variation in training load did not yield cognitive enhancements, although both protocols exhibited positive effects on brain-derived neurotrophic factor (BDNF) levels. Moreover, this study establishes a clear positive association between short-term and working memory and neurotrophic biomarkers. In addition, the independent predictive value of change in insulin-like growth factor-1 (IGF-1) on improvement in short-term and working memory highlight the close relationship between neurotrophic markers and cognition. Consequently, our results advocate for exercise training interventions targeting neurotrophic biomarkers to enhance cognitive function among individuals with coronary artery disease.

Regenerative potentials of bone marrow mesenchymal stem cells derived exosomes or its combination with zinc in recovery of degenerated circumvallate papilla following surgical bilateral transection of glossopharyngeal nerve in rats

BackgroundTaste buds’ innervation is necessary to sustain their cell turnover, differentiated taste buds and nerve fibers in circumvallate papilla (CVP) disappear following glossopharyngeal nerve transection. Normally, taste buds recover to baseline number in about 70 days. Bone marrow stem cell (BM-MSC) derived exosomes or their combination with Zinc chloride are used to assess their potential to speed up the regeneration process of CVP following bilateral deafferentation.MethodsTwenty-eight male Sprague-Dawley rats were randomly divided into four groups; Group I: subjected to sham operation followed by IP injection of saline. The other experimental groups (II, III and IV) were subjected to surgical bilateral transection of glossopharyngeal nerve. Group II received single IP injection of saline. Group III received single IV injection of BM-MSC-derived exosomes (100 µg). Group IV received single IV injection of BM-MSC-derived exosomes and single IP injection of zinc chloride (5 mg/kg). After 28 days, CVP was dissected and prepared for histological and histomorphometric analysis, RT-PCR for cytokeratin 8 gene expression, ELISA to assess protein level of brain-derived neurotrophic factor, redox state analysis of malondialdehyde and glutathione content, followed by statistical analysis.ResultsHistopathologically, group II exhibited great tissue damage with marked reduction in taste buds and signs of degeneration in the remaining ones. Group III was close to control group with marked improvement in taste buds’ number and structure. Group IV showed inferior results when compared to group III, with many immature taste buds and signs of degeneration. Statistical results showed that groups I and III have significantly higher values than groups II and IV regarding taste buds’ number, cytokeratin 8, and reduced glutathione. However, malondialdehyde demonstrated high significant values in group IV compared to groups I and III. Regarding brain-derived neurotrophic factor, group III had significantly higher values than group II.ConclusionBM-MSC-derived exosomes have superior regenerative potentials in acceleration of CVP and nerve healing following bilateral transection of glossopharyngeal nerve in contrary to its combination with zinc chloride.Graphical

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

Introduction: 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. Methods: 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). Results: the pBDNF levels were significantly higher in the MDD (p &lt; 0.001) and AD (p &lt; 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 &lt; 0.0001) and controls (exon I promoter: p = 0.0001, exon IV promoter: p &lt; 0.0001). In the patients, but not in the controls, the BDNF promoters’ methylation levels showed significant negative correlations with occupational stress. Conclusions: 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.

Efficacy of non-invasive brain stimulation for post-stroke sleep disorders: a systematic review and meta-analysis

ObjectiveThis study aimed to systematically assess the clinical efficacy of non-invasive brain stimulation (NIBS) for treating post-stroke sleep disorders (PSSD).MethodsWe conducted thorough literature search across multiple databases, including PubMed, Web of Science, EmBase, Cochrane Library, Scopus, China Biology Medicine (CBM); China National Knowledge Infrastructure (CNKI); Technology Periodical Database (VIP), and Wanfang Database, focusing on RCTs examining NIBS for PSSD. Meta-analyses were performed using RevMan 5.4 and Stata 14.ResultsEighteen articles were reviewed, including 16 on repetitive Transcranial Magnetic Stimulation (rTMS), one on Theta Burst Stimulation (TBS), and two on transcranial Direct Current Stimulation (tDCS). Meta-analysis results indicated that rTMS within NIBS significantly improved the Pittsburgh Sleep Quality Index (PSQI) score (MD = −1.85, 95% CI [−2.99, −0.71], p &amp;lt; 0.05), the 17-item Hamilton Depression Rating Scale (HAMD-17) score [MD = −2.85, 95% CI (−3.40, −2.30), p &amp;lt; 0.05], and serum brain-derived neurotrophic factor (BDNF) levels [MD = 4.19, 95% CI (2.70, 5.69), p &amp;lt; 0.05], while reducing the incidence of adverse reactions [RR = 0.36, 95% CI (0.23, 0.55), p &amp;lt; 0.05]. TBS significantly improved the PSQI score in patients with PSSD (p &amp;lt; 0.05). Conversely, tDCS significantly improved the HAMD-17 score in PSSD patients [MD = −1.52, 95% CI (−3.41, −0.64), p &amp;lt; 0.05]. Additionally, rTMS improved sleep parameters, including Stage 2 sleep (S2%) and combined Stage 3 and 4 sleep (S3 + S4%) (p &amp;lt; 0.05), while tDCS improved total sleep time (TST) and sleep efficiency (SE) (p &amp;lt; 0.05).Subgroup analysis results indicated: (1) Both LF-rTMS and HF-rTMS improved PSQI scores (p &amp;lt; 0.05). (2) Both rTMS combined with medication and rTMS alone improved PSQI scores (p &amp;lt; 0.05). Compared to the sham/blank group, the rTMS group showed improvements in SE, sleep latency (SL), S1%, S3 + S4%, and REM sleep (REM%). The rTMS combined with medication group showed improved SL compared to the medication-only group (p &amp;lt; 0.05).ConclusionNIBS effectively improves sleep quality, structure, depression levels, and BDNF levels in PSSD patients, while also being safe. Further investigations into the potential of NIBS in PSSD treatment may provide valuable insights for clinical applications.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, CRD42023485317.

Fluoxetine Ameliorates Cognitive Deficits in High-Fat Diet Mice by Regulating BDNF Expression.

High-fat diet (HFD) induced obesity is associated with depression-related behavioral and neurogenic changes and may lead to cognitive impairment. Fluoxetine (FXT), the most commonly used antidepressant, may alleviate depressive symptoms by increasing neurogenesis, but the potential efficacy of FXT for HFD-induced cognitive deficits is unclear. In this study, we established an obese HFD mouse model by feeding three-week-old male C57BL/6N mice with a chronic HFD for 18 weeks, then assessed adipose tissue morphology by magnetic resonance imaging and histopathology, assessed cognitive function by Morris water maze and novel object recognition tests, and detected DCX+ and BrdU+ expression in the hippocampal dentate gyrus (DG) region by immunofluorescence bioassay. Western blot detected brain-derived neurotrophic factor (BDNF) levels and CREB-BDNF pathway-related genes were assayed by Quantitative RT-PCR. The results of the study showed that HFD contributes to obesity and cognitive deficits, and more importantly, it also reduces BDNF expression and neurogenesis levels in the hippocampus. Subsequently, we found that treatment with FXT (10 mg/kg/day) ameliorated chronic HFD-induced cognitive deficits and increased the expression of Nestin, BrdU+, and DCX+ in the DG, restored BDNF expression in the hippocampus and increased the expression of genes related to CREB, BDNF, NGF, and MAPK1. In conclusion, our data elucidated that FXT ameliorates cognitive deficits and reduces chronic HFD-induced neurogenesis by restoring BDNF expression and CREB-BDNF signaling, this provides a good basis and scientific significance for future research on the clinical treatment of obesity.

Corticosterone-Mediated BDNF Changes and Their Effects on Adult Neurogenesis in Depression

Adult neurogenesis, the process of generating functional neurons from neural precursor cells in the adult brain, is essential for cognitive function and emotional regulation. Major Depressive Disorder (MDD), characterized by persistent sadness and decreased psychosocial function, is associated with impaired adult hippocampal neurogenesis (AHN). Elevated levels of corticosterone (CORT), a glucocorticoid released in response to stress, have been shown to downregulate brain-derived neurotrophic factor (BDNF), a crucial regulator of neurogenesis, thereby inhibiting AHN. Despite significant advances in understanding the impact of CORT and BDNF on neurogenesis, the precise molecular and cellular pathways involved remain unclear. This review highlights key gaps in the research, particularly the need for a deeper understanding of how glucocorticoid and mineralocorticoid receptors regulate BDNF transcription, the role of autophagic pathways in BDNF degradation, and the influence of glutamatergic signaling on these processes. Future research should focus on elucidating these mechanisms to develop targeted therapeutic strategies, including pharmacological interventions that modulate BDNF and CORT levels and lifestyle modifications like exercise and adequate sleep to enhance neurogenesis. Understanding these complex interactions will be crucial for advancing treatments for depression and improving mental health outcomes.

Brain-Derived Neurotrophic Factor (BDNF) is Associated with Self-Reported Cognitive Function in Adults with HIV.

Background: People with HIV (PWH) are at risk of developing HIV-associated neurocognitive disorder (HAND) despite receiving combination antiretroviral therapy. Brain-derived neurotrophic factor (BDNF) has been implicated in cognitive function and neuroplasticity, but its role in HIV-related neuroinflammation remains understudied. Methods: This study analyzed data from the CHAMPS study, assessing BDNF serum levels and cognitive function in 140 adults with HIV at baseline. Cognitive function was evaluated using the PROMIS Applied Cognition-Abilities 8-item questionnaire. BDNF levels (pg/ml) were measured using high sensitivity Enzyme-Linked Immunoassay (ELISA) kits. Linear regression analyses were conducted to explore the associations between BDNF levels, cognitive function, and AIDS diagnosis, adjusting for demographic variables. Results: A significant positive association was found between BDNF levels and cognitive function scores in PWH (p = .03). Additionally, PWH with a history of AIDS diagnosis showed significantly lower BDNF levels (p = .02). Other demographic factors did not significantly impact cognitive function or BDNF levels in this cohort. Conclusions: Our results highlight the potential of BDNF as a biomarker for cognitive decline in PWH and suggest its relevance in understanding HAND pathophysiology. Further research is warranted to explore the multifaceted interactions influencing cognitive outcomes in this population and to develop targeted interventions for improving cognitive health in PWH.

Vitamin C improved anxiety and depression like behavior induced by chronic unpredictable mild stress in adolescent rats by influencing on oxidative stress balance, neurotransmitter systems, and inflammatory response

ABSTRACT Objectives: Stress is an adaptive response to different events in daily life that could strain physically, emotionally, or psychologically. Adolescence is an important developmental period due to physical, psychological, and social maturation. The aim of our study is to state whether chronic unpredictable mild stress (CUMS) during adolescence in male rats can cause anxiety and depression in adulthood and whether vitamin C (Vit C) can prevent this problem or not. Methods: For this purpose, we performed behavioral tests, including open field test, elevated plus maze, and forced swimming test. In addition, we investigated the metabolism of serotonin, the level of inflammation, oxidative stress and brain-derived neurotrophic factor (BDNF) in the brain cortex tissue of animals. Results: Results indicated that CUMS exacerbates mood-related behaviors by affecting the brain oxidative stress balance, inflammatory response, and serotonin metabolism. Moreover, we found that CUMS-Vit C co-treatment could significantly reverse CUMS-induced complications by restoration of the mentioned biochemical parameters. Discussion: Taken together, we would like to suggest the use of Vit C supplementation as a safe, inexpensive, and effective strategy for the management of CUMS.

Neuroprotective effects of Daphnetin on hippocampal neurons and blood-brain barrier integrity in a mouse model of cerebral ischemia

The purpose of this research was to assess the impact of different doses of Daphnetin (DAP, a natural compound derived from coumarin) on hippocampus neuronal injury, neurobehavioral function, blood-brain barrier (BBB) integrity, expression of claudin-5, brain-derived neurotrophic factor (BDNF), superoxide dismutase (SOD), and inflammatory markers in a mouse model of cerebral ischemia. Cerebral ischemia was induced in mice through 30 minutes of bilateral common carotid occlusion (BCCAO), followed by 48 hours of reperfusion. The viability of hippocampal neurons was assessed using Cresyl violet staining and BBB function was determined by measuring Evans blue (E.B) dye leakage. Spatial memory was tested using the Radial Arm Water Maze (RAWM) task. Claudin-5 and BDNF were measured by immunofluorescence, while SOD, interleukin-1 beta (IL-1β), and nuclear factor-κB (NF-κB) expression were determined through western blotting. Administering DAP significantly increased neuron survival in the hippocampus CA1, CA3, and dentate gyrus (DG) regions and improved spatial memory dose-dependently (P<0.0001). Treatment with DAP (40 mg/kg IP) significantly reduced E.B leakage and brain water content (P<0.001). Furthermore, it increased the claudin-5, BDNF, and SOD levels and diminished NF-κB and IL-1β expression (P<0.0001). The research found that DAP protected neurons in the CA1, CA3, and DG areas of the hippocampus, enhanced behavioral functions, and preserved BBB integrity in a cerebral ischemia model. This positive impact is achieved by increasing the expression of claudin-5, BDNF, and SOD and diminishing neuroinflammation. Further research is required to clarify the mechanisms and possible clinical uses.

Brain-Derived Neurotrophic Factor (BDNF) as a Predictor of Treatment Response in Schizophrenia and Bipolar Disorder: A Systematic Review

Brain-derived neurotrophic factor (BDNF) is a potential biomarker of response to treatment in psychiatric disorders. As it plays a role in the pathophysiological development of schizophrenia and bipolar disorder, it is of interest to study its role in predicting therapeutic responses in both conditions. We carried out a systematic review of the literature, looking for differences in baseline BDNF levels and the Val66Met BDNF polymorphism in these disorders between responders and non-responders, and found information showing that the Val/Val genotype and higher baseline BDNF levels may be present in patients that respond successfully to pharmacological and non-pharmacological treatments. However, there is still limited evidence to support the role of the Val66Met polymorphism and baseline BDNF levels as predictors of treatment response.

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.

Executive functions in older adults with generalised anxiety disorder and healthy controls: Associations with heart rate variability, brain-derived neurotrophic factor, and physical fitness

Executive functions (EF) decline with age and this decline in older adults with generalised anxiety disorder (GAD) may be influenced by heart rate variability (HRV), brain-derived neurotrophic factor (BDNF), and physical fitness. Understanding these relationships is important for tailored treatments in this population. In this study, 51 adults with GAD (M age = 66.46, SD = 4.08) and 51 healthy controls (M age = 67.67, SD = 4.04) were assessed on cognitive inhibition (Stroop task), shifting (Trails part 4), flexibility (Wisconsin Card Sorting Test – Perseverative errors), working memory (Digit Span Backwards), IQ (Wechsler Abbreviated Scale of Intelligence), high frequency HRV, serum mature BDNF levels, and VO2 max. Results indicated that participants with GAD exhibited better cognitive inhibition compared to controls, with no general reduction in EF. Cognitive inhibition was predicted by gender, HRV, and BDNF levels, while cognitive shifting was predicted by gender and IQ, and cognitive flexibility and working memory by IQ. The enhanced cognitive inhibition in GAD participants might stem from maladaptive use of this function, characteristic of GAD, or protection from EF decline due to normal HRV. Increased BDNF levels, possibly due to good fitness, or compensatory mechanisms related to the disorder, might also play a role. These findings highlight the complexity of EF and related mechanisms in GAD, highlighting the need for interventions that consider both cognitive and physiological factors for optimal outcomes.

Brain-derived neurotrophic factor modulation in response to oxidative stress and corticosterone: role of scopolamine and mirtazapine

Major Depressive Disorder (MDD) is a very complex disease, challenging to study and manage. The complexities of MDD require extensive research of its mechanisms to develop more effective therapeutic approaches. Crucial in the context of this disease is the role of brain-derived neurotrophic factor (BDNF) signaling pathway. AimThis manuscript aims to explore the complex relationship between MDD and BDNF signaling pathway, focusing on how BDNF is modulated in response to oxidative stress and corticosterone, known to be altered in MDD and contributing to the pathology of the disorder, when treated with scopolamine and mirtazapine. MethodsTo assess BDNF levels after the different treatment conditions, rat hippocampal slices and mice primary hippocampus and cortical cell culture were analyzed by immunofluorescence and Western blot. Key findingsBoth mirtazapine and scopolamine under stress conditions induced by hydrogen peroxide (H2O2) and corticosterone, had a significant impact on BDNF levels, and this was distinct in different neuronal models. Mirtazapine, especially when combined with H2O2, altered BDNF expression. Scopolamine when combined with both stressors also altered BDNF levels. However, its effects varied depending on the specific neuronal model and stress condition. In accordance with BDNF results, phosphorylated tropomyosin receptor kinase B (pTrkB) presented increased activation when neuronal cells subjected to stress were treated with mirtazapine or scopolamine. SignificanceCollectively, this study highlights the complex connection between these compounds, stress conditions, and BDNF/TrkB modulation, supporting the potential therapeutic effects of scopolamine and mirtazapine in modulating BDNF levels, even in stressful conditions.

Effect of a 12-Week High Intensity Interval Training on Serum Brain Derived Neurotrophic Factor of Obese Undergraduates

The study investigated the effect of a 12-week High Intensity Interval Training (HIIT) on Serum Brain Derived Neurotrophic Factor (BDNF) among obese undergraduates of the University of Benin. The pretest-posttest randomized experimental design was employed for the study. The study involved a population of one hundred and twenty obese undergraduates, with a sample of twenty-four selected using simple random sampling. The participants’ anthropometric profiles were analyzed descriptively using mean and standard deviation, and the hypothesis was tested using analysis of covariance (ANCOVA) with statistical significance set at a p-value of &lt;0.05. The Bonferroni post-hoc test was conducted to pinpoint the source of the differences between the groups. The results showed a significantly higher increase in Serum BDNF levels (2.07 ± 1.9 vs. 2.38 ± 2.1) in the experimental group. This suggests that the HIIT protocol had a notable impact on the serum BDNF concentration of the obese undergraduates. Therefore, HIIT may serve as an effective intervention for elevating BDNF levels and potentially enhancing brain health. The study recommends that policymakers in Nigeria and other sub-Saharan African nations should prioritize addressing obesity due to its potential cognitive complications.

Effects of Boron on Learning and Behavioral Disorders in Rat Autism Model Induced by Intracerebroventricular Propionic Acid.

Autism spectrum disorder is a neurodevelopmental disorder in which learning, communication, and social interaction are impaired. Research has sought to minimize the neural impairments associated with autism spectrum disorder and improve the quality of life. Recent studies suggest that boron may benefit nerve cells, with effects varying depending on the dosage. This study explored the impact of boron, administered as boric acid, on behavioral, biochemical, and histopathological parameters in a rat model of autism induced by propionic acid (PPA). Thirty-two male Sprague-Dawley rats were divided into control, autism model, and boron-treated groups. Behavioral tests were conducted pre- and post-PPA induction, with brain tissue analyzed post-euthanasia. Proinflammatory cytokines (tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)) and brain-derived neurotrophic factor (BDNF) levels were assessed in the hippocampus. Histopathological evaluations were conducted on the hippocampus and cerebellum. Autism model rats displayed impaired learning, elevated BDNF and cytokine levels, microglial and astrocytic activation, and decreased Purkinje cell count. The boron-treated groups showed improvements, particularly with the 4mg/kg dose. This dose enhanced learning and social interaction, reduced proinflammatory cytokine levels, prevented microglial and astrocytic activation, and increased Purkinje cell count. Boron treatment exhibited neuroprotective potential, ameliorating autism spectrum disorder deficits by modulating cytokines, BDNF, microglia, and astrocytes, with low doses yielding pronounced effects.

Obesity Control and Supplementary Nutraceuticals as Cofactors of Brain Plasticity in Multiple Sclerosis Populations.

Multiple sclerosis (MS) is an immune-mediated disease characterized by inflammation, demyelination, and neurodegeneration within the central nervous system. Brain plasticity, the brain's ability to adapt its structure and function, plays a crucial role in mitigating MS's impact. This paper explores the potential benefits of lifestyle changes and nutraceuticals on brain plasticity in the MS population. Lifestyle modifications, including physical activity and dietary adjustments, can enhance brain plasticity by upregulating neurotrophic factors, promoting synaptogenesis, and reducing oxidative stress. Nutraceuticals, such as vitamin D, omega-3 fatty acids, and antioxidants like alpha lipoic acid, have shown promise in supporting brain health through anti-inflammatory and neuroprotective mechanisms. Regular physical activity has been linked to increased levels of brain-derived neurotrophic factor and improved cognitive function. Dietary interventions, including caloric restriction and the intake of polyphenols, can also positively influence brain plasticity. Integrating these lifestyle changes and nutraceuticals into the management of MS can provide a complementary approach to traditional therapies, potentially improving neurological outcomes and enhancing the quality of life for the MS population.

Ultra-processed foods intake in relation to metabolic health status, serum brain-derived neurotrophic factor and adropin levels in adults

BackgroundIn recent years, there has been a lot of discussion over the impact of ultra-processed foods (UPFs) intake on overall health of subjects. However, the association between UPFs intake and metabolic unhealthy (MU) status is still in a state of ambiguity. The current study assessed the relationship between UPFs intake and MU status with regard to brain-derived neurotrophic factor (BDNF) and adropin levels.MethodsA sample of Iranian adults (aged 20–65 years) was selected to participate in this cross-sectional study using a multistage cluster random-sampling method. UPFs intake was assessed by a validated food frequency questionnaire and NOVA classification. Concentrations of metabolic parameters, BDNF and adropin were determined through fasting blood samples. MU status was assessed according to the criteria proposed by Wildman.ResultsThe overall prevalence of MU phenotype among study participants (n = 527) was 42.5%. Higher intake of UPFs was associated with elevated odds of MU status in multivariable-adjusted model (ORT3 vs. T1=1.88; 95%CI: 1.02–3.45). Moreover, a positive association was observed between UPFs intake and hypertriglyceridemia after controlling all confounders (ORT3 vs. T1=2.07; 95%CI: 1.15–3.73). However, each tertile increase in UPFs intake was not significantly associated with serum BDNF (\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\:\\beta\\:$$\\end{document}=0.15; 95%CI: -0.05, 0.34; P = 0.14) and adropin (\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\:\\beta\\:$$\\end{document}=-1.37; 95%CI: -6.16, 3.42; P = 0.58) levels in multivariable-adjusted linear regression models.ConclusionOur findings suggested that higher consumption of UPFs was related to increased likelihood of MU status among a sample of Iranian adults. Further longitudinal studies are needed to verify the directionality and generalizability of the results to all adult populations.