Researchers have reported that serum brain-derived neurotrophic factor (sBDNF) of drug-free depressed patients are lower than those of healthy controls and proposed that low sBDNF levels might reflect
Experimental evidence in mice indicates that environmental conditions affect females and males differently. However, in a recent study analyzing the heterozygous mutation of brain-derived neurotrophic factor (BDNF), both sexes presented a similar emotional phenotype, which became obvious only under impoverished, but not in enriched conditions suggesting an enrichment-induced rescue. To investigate the basis of this behavioral rescue effect, we analyzed neurochemical changes (BDNF expression, serotonergic changes, and corticosterone) in the hippocampus, frontal cortex and hypothalamus of animals housed under respective conditions. In male mice, enrichment induced an increase of BDNF expression in the hippocampus of both BDNF heterozygous (BDNF(+/-)) and wild-types. Notably, in enriched-reared BDNF(+/-) mice BDNF mRNA and protein increased to levels comparable to those of wild-types in impoverished environment. In the frontal cortex of males, only wild-types presented an enrichment-induced increase of
Exercise is recognized as a promising approach to counteract aging-associated declines in cognitive functions. However, the exact molecular pathways involved remain unclear. Aerobic training interventions and improvements in peak oxygen uptake (VO2peak) have been associated with increases in the peripheral concentration of brain-derived neurotrophic factor (BDNF) and better cognitive performances. However, other training interventions such as resistance training and gross motor skills programs were also linked with improvements in cognitive functions. Thus far, few studies have compared different types of physical exercise training protocols and their impact on BDNF concentrations, especially in participants over 60 years old. The main objective of this study was to compare the effects of three exercise protocols on plasma BDNF concentrations at rest in healthy older adults. Thirty-four older adults were randomized into three interventions: (1) lower body strength and aerobic training (LBS-A), (2) upper
Fig. 6 HSP105-siRNA in HT22 cells or stressed mouse brain decreased BDNF levels and abolished antidepressant effects.. (A) Level of HSP105 mRNA in HT22 cells (ANOVA, F2,13 = 544.1, n = 5 to 6). (B) Level of BDNF mRNA in HT22 cells (ANOVA, F2,13 = 10.74, n = 5 to 6). (C) The level of HSP105 protein in the hippocampus was detected by Western blotting (n = 3). (D) Immobility times in the forced swim test (ANOVA, F2,11 = 6.03). (E) Immobility times in the tail suspension test (ANOVA, F2,11 = 15.02). (F) Social interaction rate in the interaction test (ANOVA, F2,11 = 5.00). (G) Sucrose preference and total fluid intake in the sucrose preference test. (H) Level of BDNF mRNA and protein in the mouse hippocampus (ANOVA, F2,11 = 4.54 and F2,12 = 5.41, respectively) (n = 4 to 5 animals per group). Each bar indicates the mean ± SEM. GGA + NTC, GGA with nontargeting control; GGA + HSP105-siRNA, GGA with HSP105-siRNA treatment. Statistically different groups are indicated by letters. ...
Background: Brain-derived neurotrophic factor (BDNF) mutant mice show hyperphagia and hyperleptinemia. Animal and cell-culture experiments suggest multiple interrelations between BDNF and the serotonin (5-HT) system. We studied serum BDNF in patients with anorexia nervosa and its associations with peripheral indicators of the 5-HT system. To control for secondary effects of acute malnutrition, we assessed acutely underweight patients with anorexia nervosa (acAN) in comparison to long-term weight-recovered patients with the disorder (recAN) and healthy controls.. Methods: We determined serum BDNF, platelet 5-HT content and platelet 5-HT uptake in 33 patients in the acAN group, 20 patients in the recAN group and 33 controls. Plasma leptin served as an indicator of malnutrition.. Results: Patients in the acAN group were aged 14-29 years and had a mean body mass index (BMI) of 14.9 (standard deviation [SD] 1.4) kg/m2. Those in the recAN group were aged 15-29 years and had a mean BMI of 20.5 (SD 1.3) ...
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Objective It is important to predict a response to an antidepressant in early time after starting the antidepressant. We previously reported that serum brain-derived neurotrophic factor (BDNF) levels in responders to treatment with antidepressants were increased, whereas, those in nonresponders were not. Therefore, we hypothesized that the changes in serum levels of BDNF from baseline (TO) to 4 weeks (T4) after treatment with selective serotonin reuptake inhibitors (SSRIs) predict the response to the treatment at 8 weeks (T8) in depressed patients. To confirm the hypothesis, we measured serum BDNF at TO, T4, and T8 during the treatment with SSRIs (paroxetine, sertraline, and fluvoxamine). Methods One hundred fifty patients (M/F; 51/99, age; 50.4 +/- 15.1 years) met major depressive disorder (MDD) using by DSM-IV-TR enrolled in the present study. We measured serum BDNF concentrations at TO, T4, and T8 in patients with MDD treated with SSRIs. Results The changes in serum BDNF, age, sex, dose of SSRIs, and
BDNF and VEGF were analyzed as continuous variables. VEGF values were log-transformed to normalize the skewed distribution of VEGF. We used Cox-proportional hazards models to relate baseline serum BDNF and logVEGF levels (separately) to risk of incident stroke/TIA in Study Sample 1. We first examined the linear effect of a 1-SD unit increase/decrease in BDNF and logVEGF on risk of stroke/TIA. We also explored threshold effects comparing the risk across quartiles of BDNF and VEGF. We observed a threshold effect with BDNF only. Therefore, we ran threshold models for BDNF using the lowest quartile, Q1, as the reference and also assessed a threshold model comparing risk for persons in Q1 with persons in Q2 to Q4. We performed a similar set of analyses on a Study Sample 1b with stroke alone as the outcome. Using multivariable linear and logistic regression models, we examined the cross-sectional associations between BDNF and logVEGF and markers of brain aging (WMHV, and VR-d and Trails B-A ...
TY - JOUR. T1 - Brain-derived neurotrophic factor promoter methylation and cortical thickness in recurrent major depressive disorder. AU - Na, Kyoung Sae. AU - Won, Eunsoo. AU - Kang, June. AU - Chang, Hun Soo. AU - Yoon, Ho-Kyoung. AU - Tae, Woo Suk. AU - Kim, Yong Ku. AU - Lee, Min-Soo. AU - Joe, Sook Haeng. AU - Kim, Hyun. AU - Ham, Byung-Joo. PY - 2016/2/15. Y1 - 2016/2/15. N2 - Recent studies have reported that methylation of the brain-derived neurotrophic factor (BDNF) gene promoter is associated with major depressive disorder (MDD). This study aimed to investigate the association between cortical thickness and methylation of BDNF promoters as well as serum BDNF levels in MDD. The participants consisted of 65 patients with recurrent MDD and 65 age-and gender-matched healthy controls. Methylation of BDNF promoters and cortical thickness were compared between the groups. The right medial orbitofrontal, right lingual, right lateral occipital, left lateral orbitofrontal, left pars ...
One of the heavy progressive vascular complications of type 2 diabetes is a central nervous system, manifesting cognitive dysfunction due to metabolic changes. Goal. Defining the role of brain-derived neurotrophic factor (BDNF) in the diagnosis of cognitive dysfunction in patients with type 2 diabetes. Materials and methods. The study involved 83 patients with type 2 diabetes at the age of 40 - 70 years. Complex examination included clinical and laboratory examination, neuropsychological testing. To screen for cognitive impairment used the Montreal Cognitive Assessment Scale (MOS test). To identify early markers of cognitive impairment was determined the level of brain-derived neurotrophic factor (BDNF). Results. The study found a negative correlation between the level of BDNF and the HbA1c (r = - 0,494, p = 0.01), fasting glucose (r = - 0,499, p = 0.01), and a positive relationship between the level of BDNF and cognitive function in patients with type 2 diabetes. Conclusion. In patients with ...
Background Following voxel-based morphometry (VBM), brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) has been shown to affect human brain morphology in Caucasians. However, little is known about the specific role of the Met/Met genotype on brain structure. Moreover, the relationship between BDNF Val66Met polymorphism and Chinese brain morphology has not been studied. Methodology/Principal Findings The present study investigated brain structural differences among three genotypes of BDNF (rs6265) for the first time in healthy young Chinese adults via cortical thickness analysis and VBM. Brain differences in Met carriers using another grouping method (combining Val/Met and Met/Met genotypes into a group of Met carriers as in most previous studies) were also investigated using VBM. Dual-approach analysis revealed less gray matter (GM) in the frontal, temporal, cingulate and insular cortices in the Met/Met group compared with the Val/Val group (corrected, P|0.05). Areas with less GM
Citation: Khundakar, A.A. and Zetterström, T.S.C. (2011) Effects of GABAB ligands alone and in combination with paroxetine on hippocampal BDNF gene expression. European Journal of Pharmacology, 671 (1-3) pp. 33-38 ...
TY - JOUR. T1 - Brain-derived neurotrophic factor is required for normal development of the central respiratory rhythm in mice. AU - Balkowiec, Agnieszka. AU - Katz, David M.. PY - 1998/7/15. Y1 - 1998/7/15. N2 - 1. Molecular mechanisms underlying maturation of the central respiratory rhythm are largely unknown. Previously, we found that brain-derived neurotrophic factor (BDNF) is required for expression of normal breathing behaviour in newborn mice, raising the possibility that maturation of central respiratory output is dependent on BDNF. 2. Respiratory activity was recorded in vitro from cervical ventral roots (C1 or C4) using the isolated brainstem-spinal cord preparation from postnatal day (P) 0.5-2.0 and P4.5 wild-type mice and mice lacking functional bdnf alleles. 3. Loss of one or both bdnf alleles resulted in an approximately 50% depression of central respiratory frequency compared with wild-type controls. In addition, respiratory cycle length variability was 214% higher in bdnf null ...
A Val66Met single-nucleotide polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene impairs activity-dependent BDNF release in cultured hippocampal neurons and predicts impaired memory and exaggerated basal hippocampal activity in healthy humans. Several clinical genetic association studies along with multi-modal evidence for hippocampal dysfunction in schizophrenia indirectly suggest a relationship between schizophrenia and genetically determined BDNF function in the hippocampus. To directly test this hypothesized relationship, we studied 47 medication-free patients with schizophrenia or schizoaffective disorder and 74 healthy comparison individuals with genotyping for the Val66Met SNP and [15O]H2O positron emission tomography (PET) to measure resting and working memory-related hippocampal regional cerebral blood flow (rCBF). In patients, harboring a Met allele was associated with significantly less hippocampal rCBF. This finding was opposite to the genotype effect seen in healthy
The neurotrophin brain-derived neurotrophic factor (BDNF) plays a key role in synaptic plasticity, in part due to changes in local protein synthesis. Activation of TrkB (tropomyosin-related kinase B) receptors for BDNF triggers several parallel signaling pathways, including the Ras/ERK, the phosphatidylinositol 3-kinase (PI3-K) and the phospholipase C-γ pathways. Recent studies have elucidated some of the signaling mechanisms that contribute to the regulation of translation activity by BDNF, through modulation of initiation and elongation phases, but the resulting changes in the proteome are not yet fully characterized. The proteins synthesized in response to activation of TrkB receptors by BDNF depend on the mRNAs that are available locally, after delivery and transport along dendrites. Recent studies have shown that BDNF may also play a regulatory role at this level. Furthermore, BDNF regulates transcription activity, thereby affecting the array of mRNAs available to be transported along dendrites.
Brain-derived neurotrophic factor (BDNF) promotes several functions in neurons and modulates neurotransmissions, especially in hippocampal regions. Frontotemporal lobar degeneration (FTLD) has a strong genetic background, but genetic risk factors ass
Context: Brain-derived neurotrophic factor (BDNF) is a pleiotropic peptide also involved in maintaining endothelial integrity. It is unknown if circulating BDNF levels are associated with risk of cardiovascular disease (CVD).. Objective: To investigate the association of circulating BDNF with CVD risk Design, Setting and Participants: First, we prospectively investigated the association of circulating BDNF levels with cardiovascular events and mortality in the 3,687 participants (mean age 65 years, 2,068 women) from the Framingham Heart Study (FHS). Next, we evaluated the association of a common nonsynonymous SNP in the BDNF gene (rs6265) with circulating BDNF concentrations in FHS. Finally, we performed a Mendelian randomization experiment in the CARDIoGRAM consortium (,22,000 coronary artery disease [CAD] cases, ,60,000 controls) to investigate whether the same SNP was associated with CAD risk in CARDioGRAM and if so, whether the direction and effect size differed from that predicted based on ...
Author(s): Bamji, Shernaz X; Rico, Beatriz; Kimes, Nikole; Reichardt, Louis F | Abstract: Neurons of the vertebrate central nervous system have the capacity to modify synapse number, morphology, and efficacy in response to activity. Some of these functions can be attributed to activity-induced synthesis and secretion of the neurotrophin brain-derived neurotrophic factor (BDNF); however, the molecular mechanisms by which BDNF mediates these events are still not well understood. Using time-lapse confocal analysis, we show that BDNF mobilizes synaptic vesicles at existing synapses, resulting in small clusters of synaptic vesicles splitting away from synaptic sites. We demonstrate that BDNFs ability to mobilize synaptic vesicle clusters depends on the dissociation of cadherin-beta-catenin adhesion complexes that occurs after tyrosine phosphorylation of beta-catenin. Artificially maintaining cadherin-beta-catenin complexes in the presence of BDNF abolishes the BDNF-mediated enhancement of synaptic vesicle
Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also appears to function downstream of the leptin-melanocortin signaling pathway to control appetite. In both animals and humans, diminished BDNF function is associated with hyperphagia, obesity, and neurocognitive deficits. We propose to study BDNF in two hyperphagic disorders: Prader-Willi syndrome and MC4R function-altering mutations. We hypothesize that patients with PWS may have increased BDNF during infancy, followed by a decline in BDNF that precedes the onset of hyperphagia and persists after the onset of obesity. We hypothesize that patients with MC4R mutations will have decreased BDNF, the severity of which will be associated with the degree of MC4R functional loss caused by the specific mutation(s) in each individual. To test these hypotheses, we wish to conduct cross-sectional studies to evaluate serum BDNF concentrations, metabolism, body composition, and ...
Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also appears to function downstream of the leptin-melanocortin signaling pathway to control appetite. In both animals and humans, diminished BDNF function is associated with hyperphagia, obesity, and neurocognitive deficits. We propose to study BDNF in two hyperphagic disorders: Prader-Willi syndrome and MC4R function-altering mutations. We hypothesize that patients with PWS may have increased BDNF during infancy, followed by a decline in BDNF that precedes the onset of hyperphagia and persists after the onset of obesity. We hypothesize that patients with MC4R mutations will have decreased BDNF, the severity of which will be associated with the degree of MC4R functional loss caused by the specific mutation(s) in each individual. To test these hypotheses, we wish to conduct cross-sectional studies to evaluate serum BDNF concentrations, metabolism, body composition, and ...
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Figure 4. Hippocampus and Perirhinal cortex in Human Brain (Figure Source). Some studies measured serum BDNF levels instead of specifically measuring brain BDNF concentration.[21][31][32][13] Serum BDNF is measured instead of brain levels because it can be measured without sacrificing the animal and is also acceptable for human studies. Acute changes in serum BDNF levels are thought to directly reflect changes in brain BDNF concentration[21][24]. There are several reasons for this: rat studies show correlations between serum and brain BDNF levels,[21] BDNF easily travels in both directions across the blood-brain barrier,[21][24] and both serum and brain BDNF levels are significantly reduced in AD.[24] There is conflicting evidence concerning exercise and its impact on serum BDNF.[24] Acute bouts of exercise have been found to increase serum BDNF levels,[21][24] but several studies have concluded that regular (chronic) exercise may lead to decreased serum BDNF levels compared to sedentary ...
The Effects of Voluntary, Involuntary, and Forced Exercises on Brain-Derived Neurotrophic Factor and Motor Function Recovery: A Rat Brain Ischemia Model - free full-text /PMC3035657/ - Feb 2011 I was happy to find that what I have personally experienced has been proven to be true: forced exercise is not as beneficial as voluntary. Sometimes science…
Environmental enrichment (EE) refers to the provision of a complex and stimulating housing condition which improves well-being, behaviour and brain function of laboratory animals. The mechanisms behind these beneficial effects of EE are only partially understood. In the current report, we describe a link between EE and neuropeptide Y (NPY), based on findings from NPY knockout (KO) mice exposed to EE. Relative to EE-housed wildtype (WT) animals, NPY KO mice displayed altered behaviour as well as molecular and morphological changes in amygdala and hippocampus. Exposure of WT mice to EE reduced anxiety and decreased central glucocorticoid receptor expression, effects which were absent in NPY KO mice. In addition, NPY deletion altered the preference of EE items, and EE-housed NPY KO mice responded to stress with exaggerated hyperthermia, displayed impaired spatial memory, had higher hippocampal brain-derived neurotrophic factor mRNA levels and altered hippocampal synaptic plasticity, effects which were not
Sigma-Aldrich offers abstracts and full-text articles by [Erica D Smith, G Aleph Prieto, Liqi Tong, Ilse Sears-Kraxberger, Jeffrey D Rice, Oswald Steward, Carl W Cotman].
The brain-derived neurotrophic factor (BDNF) is essential for the survival of neurons in the central nervous system (CNS). The expression of BDNF is regulated by several conditions related to neuronal activity including seizures, normal neuronal depolarization, and long-term potentiation (LTP)--all mechanisms that increase intracellular concentrations of calcium. Increased calcium leads to the occupation of calcium-adenosine-3′,5′-monophosphate (cAMP) response element (CRE) in the BDNF promoter by transcription factors of the CRE-binding protein (CREB) family. The BDNF gene contains four noncoding exons located 5′ to the coding region, each of which can be alternatively spliced to the 3′ coding exon. BDNF mRNAs that contain the nontranslated exon 3 are the most highly expressed isoform in response to membrane depolarization. In an attempt to understand the processes that contribute to activity-induced neuronal gene-expression, Tao et al. have identified a new mechanism by which BDNF ...
Brain-Derived Neurotrophic Factor: A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)
Background: Brain-derived neurotrophic factor (BDNF) is associated with coronary artery diseases. However, its role and mechanism in myocardial infarction (MI) is not fully understood. Methods: ...
Human neural stem cells genetically modified to overexpress brain-derived neurotrophic factor promote functional recovery and neuroprotection in a mouse stroke model. - Hong J Lee, In J Lim, Min C Lee, Seung U Kim
The role of brain-derived neurotrophic factor in the regulation of cell growth and gene expression in melanotrope cells of Xenopus laevis Academic Article ...
Neurotrophic factors are critical regulators of the formation and plasticity of neuronal networks. Brain-derived neurotrophic factor (BDNF) is abundant in the brain and periphery, and is found in both human serum and plasma. Animal studies have demonstrated that stress reduces BDNF expression or activity in the hippocampus and that this reduction can be prevented by treatment with antidepressant drugs. A similar change in BDNF activity occurs in the brain of patients with major depression disorder (MDD). Recently, clinical studies have indicated that serum or plasma BDNF levels are decreased in untreated MDD patients. Antidepressant treatment for at least four weeks can restore the decreased BDNF function up to the normal value. Therefore, MDD is associated with impaired neuronal plasticity. Suicidal behavior can be a consequence of severe impaired neuronal plasticity in the brain. Antidepressant treatment promotes increased BDNF activity as well as several forms of neuronal plasticity, ...
Have you ever heard the term "runners high?" Is it really possible to feel that good, just from exercise? You bet it is. Exercise can activate the same pathways in the brain as morphine and increases the release of endorphins, natural feel-good neurotransmitters. That makes exercise the closest thing to a happiness pill you will ever find.. Boost your mood. Physical exercise stimulates neurotransmitter activity-specifically norepinephrine, dopamine, and serotonin-which elevates mood.. Fight depression. Exercise can be as effective as prescription medicine in treating depression. One of the reasons why exercise can be so useful is because it increases brain-derived neurotrophic factor (BDNF).. BDNF is like an anti-aging wonder drug that is involved with the growth of new brain cells. Think of BDNF as a sort of Miracle-Gro for your brain. BDNF not only grows new brain cells, but it is also instrumental in putting the brakes on depression.. The antidepressant benefits of exercise have been well ...
i] Ravindran P.N., Babu K.N., Sivaraman K. "Turmeric: The Genus Curcuma"; CRC Press Pg 5 March 1, 2007 ISBN 9780849370342 (source). [ii] "Tumeric" US National Library of Medicine ncbi.nlm.hih.gov Retrieved August 4, 2016 (source). [iii] "Turmeric" National Center for Complementary and Integrative Health nih.gov (source). [iv] Ng T.P., Chiam P.C., Lee T., Chua H.C., Lim L., Kua E.H. "Curry consumption and cognitive function in the elderly." American Journal of Epidemiology. 2006 Nov 1;164(9):898-906. (source). [v] Kulkarni S.K., Dhir A. "An Overview of Curcumin in Neurological Disorders" Indian Journal of Pharmaceutical Sciences. 2010 Mar-Apr; 72(2): 149-154. (source). [vi] Wang R., Li Y.B., Li Y.H., Xu Y., Wu H.L., Li X.J. "Curcumin protects against glutamate excitotoxicity in rat cerebral cortical neurons by increasing brain-derived neurotrophic factor level and activating TrkB."Brain Research. 2008 May 19;1210:84-91. (source). [vii] Kim S.J., Son T.G., Park H.R., Park M., Kim M.S., Kim H.S., ...
i] Ravindran P.N., Babu K.N., Sivaraman K. "Turmeric: The Genus Curcuma"; CRC Press Pg 5 March 1, 2007 ISBN 9780849370342 (source). [ii] "Tumeric" US National Library of Medicine ncbi.nlm.hih.gov Retrieved August 4, 2016 (source). [iii] "Turmeric" National Center for Complementary and Integrative Health nih.gov (source). [iv] Ng T.P., Chiam P.C., Lee T., Chua H.C., Lim L., Kua E.H. "Curry consumption and cognitive function in the elderly." American Journal of Epidemiology. 2006 Nov 1;164(9):898-906. (source). [v] Kulkarni S.K., Dhir A. "An Overview of Curcumin in Neurological Disorders" Indian Journal of Pharmaceutical Sciences. 2010 Mar-Apr; 72(2): 149-154. (source). [vi] Wang R., Li Y.B., Li Y.H., Xu Y., Wu H.L., Li X.J. "Curcumin protects against glutamate excitotoxicity in rat cerebral cortical neurons by increasing brain-derived neurotrophic factor level and activating TrkB."Brain Research. 2008 May 19;1210:84-91. (source). [vii] Kim S.J., Son T.G., Park H.R., Park M., Kim M.S., Kim H.S., ...
The proliferation, differentiation and survival of neuronal and glial cells are affected by a number of neurotrophic factors, such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and others. In a previous study, we observed the effects of `SEMAX® (Met-Glu-His-Phe-Pro-Gly-Pro), the physiologically active analogue of adrenocorticotropic hormone(4-10), on neuronal cell survival in vitro. We hypothesized that these effects may be mediated by the regulation of expression of some neurotrophic factors. To test this hypothesis we analyzed NGF and BDNF gene expression in glial cells obtained from the basal forebrain of newborn rats, following in vitro treatment with `SEMAX®. We observed changes in mRNA levels for both the NGF and BDNF genes. The greatest increase in expression was found after 30 min of `SEMAX® administration. At this time, BDNF mRNA level was increased eight-fold in comparison with control, and NGF mRNA level was increased five-fold. 2001 Elsevier Science ...
Our results demonstrate that genetic loss of MeCP2 is associated not only with deficits in neuronal BDNF content but also with a significant increase in the percentage of BDNF content available for release. Because deficits in BDNF protein levels are temporally regulated in a cell-type- or region-specific manner, the net effect of the Mecp2 −/y mutation on BDNF release will vary among neuronal populations and with age. The fact that newborn Mecp2 −/y neurons release abnormally high levels of BDNF raises the possibility that BDNF-dependent regulation of neural development is disrupted in mutant mice in vivo. For example, hypersecretion of BDNF, particularly by newborn Mecp2 −/y neurons at rest, could derange developmental processes that depend on tight coupling between neuronal activity and BDNF release, such as activity-dependent refinement of synaptic connections (Lein and Shatz, 2000). Additional studies are required to determine how the Mecp2 −/y mutation affects evoked release at ...
Executive function declines with age, but engaging in aerobic exercise may attenuate decline. One mechanism by which aerobic exercise may preserve executive function is through the up-regulation of brain-derived neurotropic factor (BDNF), which also declines with age. The present study examined BDNF as a mediator of the effects of a 1-year walking intervention on executive function in 90 older adults (mean age = 66.82). Participants were randomized to a stretching and toning control group or a moderate intensity walking intervention group. BDNF serum levels and performance on a task-switching paradigm were collected at baseline and follow-up. We found that age moderated the effect of intervention group on changes in BDNF levels, with those in the highest age quartile showing the greatest increase in BDNF after 1-year of moderate intensity walking exercise (p = .036). The mediation analyses revealed that BDNF mediated the effect of the intervention on task-switch accuracy, but did so as a function of
article{1fdd16d8-cade-46c6-b3bf-0719173f035c, abstract = {Both brain-derived neurotrophic factor (BDNF) and the serotonin receptor 2A (5-HT2A) have been related to depression pathology. Specific 5-HT2A receptor changes seen in BDNF conditional mutant mice suggest that BDNF regulates the 5-HT2A receptor level. Here we show a direct effect of BDNF on 5-HT2A receptor protein levels in primary hippocampal neuronal and mature hippocampal organotypic cultures exposed to different BDNF concentrations for either 1, 3, 5 or 7 days. In vivo effects of BDNF on hippocampal 5-HT2A receptor levels were further corroborated in (BDNF +/-) mice with reduced BDNF levels. In primary neuronal cultures, 7 days exposure to 25 and 50 ng/mL BDNF resulted in downregulation of 5-HT2A, but not of 5-HT1A, receptor protein levels. The BDNF-associated downregulation of 5-HT2A receptor levels was also observed in mature hippocampal organotypic cultures, excluding confounding effects of BDNF on immature tissue. BDNF +/- mice ...
Brain-derived neurotrophic factor (BDNF) is a key player in synaptic plasticity, and consequently, learning and memory. Because of its fundamental role in numerous neurological functions in the central nervous system, BDNF has utility as a biomarker and drug target for neurodegenerative and neuropsychiatric disorders. Here, we generated a screening assay to mine inducers of Bdnf transcription in neuronal cells, using primary cultures of cortical cells prepared from a transgenic mouse strain, specifically, Bdnf-Luciferase transgenic (Bdnf-Luc) mice. We identified several active extracts from a library consisting of 120 herbal extracts. In particular, we focused on an active extract prepared from Ginseng Radix (GIN), and found that GIN activated endogenous Bdnf expression via cAMP-response element-binding protein-dependent transcription. Taken together, our current screening assay can be used for validating herbal extracts, food-derived agents, and chemical compounds for their ability to induce Bdnf
BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF). BDNF is the dominant factor (compared to other neurotrophic factors) in the brain. This holds true not only to the variety of brain structures, but also to the BDNF expression level. According to our data [16, 17], BDNF expression in the brain structures of rats is much higher than that of GDNF. According to current estimations, the human BDNF gene is located in the p14 region of chromosome 11 (in rats and mice these are chromosomes 3q33 and 2qE3, respectively) and contains 12 exons, nine of which have specific promoters (I-VIII 5′ exons spliced to the common 3′ IX exon). This gene structure is observed both in humans [18] and in rodents [19], but the number of exons varies (9 in mice and 10 in rats). Transcripts of template RNA as well as BDNF protein are widely present in the neocortex, hippocampus, amygdala, and cerebellum [20].. BDNF is notable by structural and functional complexity, which is based on (i) the presence of several promoters in the ...
Authors: GV Brierley, IK Priebe, L Purins, KYC Fung, B Tabor, T Lockett, E Nice, P Gibbs, J Tie, P McMurrick, J Moore, A Ruszkiewicz, A Burgess, LJ Cosgrove
The response of embryonic chick nodose ganglion (neural placode-derived) and dorsal root ganglion (neural crest-derived) sensory neurons to the survival and neurite-promoting activity of brain-derived neurotrophic factor (BDNF) was studied in culture. In dissociated, neuron-enriched cultures established from chick embryos between Day 6 (E6) and Day 12 (E12) of development, both nodose ganglion (NG) and dorsal root ganglion (DRG) neurons were responsive on laminin-coated culture dishes to BDNF. In the case of NG, BDNF elicited neurite outgrowth from 40 to 50% of the neurons plated at three embryonic ages; E6, E9, and E12. At the same ages, nerve growth factor (NGF) alone or in combination with BDNF, had little or no effect upon neurite outgrowth from NG neurons. The response of NG neurons to BDNF was dose dependent and was sustainable for at least 7 days in culture. Surprisingly, in view of a previous study carried out using polyornithine as a substrate for neuronal cell attachment, on ...
BDNF antibody (brain-derived neurotrophic factor) for ELISA. Anti-BDNF pAb (GTX17884) is tested in Human, Mouse samples. 100% Ab-Assurance.
OBJECTIVE: To evaluate whether an animal model of mania induced by lisdexamfetamine dimesylate (LDX) has an inflammatory profile and whether immune activation by lipopolysaccharides (LPS) has a cumulative effect on subsequent stimuli in this model. We also evaluated the action of lithium (Li) on inflammatory and neurotrophic factors. METHODS: Adult male Wistar rats were subjected to an animal model of mania. After the open-field test, they were given LPS to induce systemic immune activation. Subsequently, the animals blood was collected, and their serum levels of brain-derived neurotrophic factor and inflammatory markers (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-1β, IL-10, and inducible nitric oxide synthase [iNOS]) were measured. RESULTS: LDX induced hyperactivity in the animals, but no inflammatory marker levels increased except brain-derived neurotrophic factor (BDNF). Li had no effect on serum BDNF levels but prevented iNOS levels from increasing in animals subjected to immune
Several studies have recently reported that chromatin-modifying mechanisms are involved in learning and memory processes in adult neurons.3,5,35 For example, Levenson et al.35 showed that whereas histone H3 was acetylated following contextual FC in the hippocampus, histone H4 was acetylated following a latent inhibition protocol for contextual FC. Lubin et al.3 investigated histone modifications at specific BDNF promoters after contextual FC. They observed a selective increase in histone H3 acetylation at the BDNF gene promoter of exon IV, and a selective decrease in histone H4 acetylation at the BDNF promoter of exon II. In our study, SPS rats demonstrated a significant increase relative to sham rats in the levels of acetylated H3 and H4 at BDNF promoters of exons I and IV after FC. In addition, this selective increase in histone acetylation at the promoters of exons I and IV were consistent with up-regulation in exon I and IV mRNA transcription associated with FC. Interestingly, there were no ...
trkB is a tyrosine protein kinase gene highly related to trk, a proto-oncogene that encodes a receptor for nerve growth factor (NGF) and neurotrophin-3 (NT-3). trkB expression is confined to structures of the central and peripheral nervous systems, suggesting it also encodes a receptor for neurotrop …
OBJECTIVE: Cross-sectional genetic association studies have reported equivocal results on the relationship between the brain-derived neurotrophic factor (BDNF) Val66Met and risk of Alzheimers disease (AD). As AD is a neurodegenerative disease, genetic influences may become clearer from prospective study. We aimed to determine whether BDNF Val66Met polymorphism influences changes in memory performance, hippocampal volume, and Aβ accumulation in adults with amnestic mild cognitive impairment (aMCI) and high Aβ. METHODS: Thirty-four adults with aMCI were recruited from the Australian, Imaging, Biomarkers and Lifestyle (AIBL) Study. Participants underwent PiB-PET and structural MRI neuroimaging, neuropsychological assessments and BDNF genotyping at baseline, 18 month, and 36 month assessments. RESULTS: In individuals with aMCI and high Aβ, Met carriers showed significant and large decline in episodic memory (d = 0.90, p = .020) and hippocampal volume (d = 0.98, p = .035). BDNF Val66Met was ...
... content are included within this article. axis prior to intracisternal infection with live meningitis, Brain-derived neurotrophic factor, Neuroinflammation, Hippocampal apoptosis Background Bacterial meningitis is a severe infection of the central nervous systems (CNS), with an annual occurrence of 0.9 per 100,000 Dasatinib biological activity people in developing countries [1, 2]. The most common causative agent is meningitis. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic family, which plays an important role in the development, differentiation, and survival of neurons in the CNS [11, 12]. BDNF exerts neuroprotective effects in multiple CNS diseases following its high-affinity binding to tropomyosin-receptor kinase B (TrkB) [13, 14]. In recent years, significant effort has been expended to identify the neuroprotective effects of BDNF on meningitis in both animal experiments and ...
R&D Systems GMP Human BDNF protein (248-GMP) is manufactured in our ISO-certified facility, lot-to-lot consistency, over 97% purity. Reproducible results in bioactivity assays. Learn More...
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