Relevant bibliographies by topics / BDNF

Academic literature on the topic 'BDNF'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 March 2024

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Journal articles on the topic "BDNF"

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Degos, Vincent, Tifenn Le charpentier, Vibol Chhor, Olivier Brissaud, Sophie Lebon, Leslie Schwendimann, Nathalie Bednareck, Sandrine Passemard, Jean Mantz, and Pierre Gressens. "Neuroprotective Effects of Dexmedetomidine against Glutamate Agonist-induced Neuronal Cell Death Are Related to Increased Astrocyte Brain-derived Neurotrophic Factor Expression." Anesthesiology 118, no. 5 (May 1, 2013): 1123–32. http://dx.doi.org/10.1097/aln.0b013e318286cf36.

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Abstract Background: Brain-derived neurotrophic factor (BDNF) plays a prominent role in neuroprotection against perinatal brain injury. Dexmedetomidine, a selective agonist of α2-adrenergic receptors, also provides neuroprotection against glutamate-induced damage. Because adrenergic receptor agonists can modulate BDNF expression, our goal was to examine whether dexmedetomidine’s neuroprotective effects are mediated by BDNF modulation in mouse perinatal brain injury. Methods: The protective effects against glutamate-induced injury of BDNF and dexmedetomidine alone or in combination with either a neutralizing BDNF antibody or an inhibitor of the extracellular signal-regulated kinase pathway (PD098059) were compared in perinatal ibotenate-induced cortical lesions (n = 10–20 pups/groups) and in mouse neuronal cultures (300 μm of ibotenate for 6 h). The effect of dexmedetomidine on BDNF expression was examined in vivo and in vitro with cortical neuronal and astrocyte isolated cultures. Results: Both BDNF and dexmedetomidine produced a significant neuroprotective effect in vivo and in vitro. Dexmedetomidine enhanced Bdnf4 and Bdnf5 transcription and BDNF protein cortical expression in vivo. Dexmedetomidine also enhanced Bdnf4 and Bdnf5 transcription and increased BDNF media concentration in isolated astrocyte cultures but not in neuronal cultures. Dexmedetomidine’s protective effect was inhibited with BDNF antibody (mean lesion size ± SD: 577 ± 148 μm vs. 1028 ± 213 μm, n = 14–20, P < 0.001) and PD098059 in vivo but not in isolated neuron cultures. Finally, PD098059 inhibited the increased release of BDNF induced by dexmedetomidine in astrocyte cultures. Conclusion: These results suggest that dexmedetomidine increased astrocyte expression of BDNF through an extracellular signal-regulated kinase-dependent pathway, inducing subsequent neuroprotective effects.
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Ding, Baojin, Paul R. Dobner, Debra Mullikin-Kilpatrick, Wei Wang, Hong Zhu, Chi-Wing Chow, John W. Cave, Richard M. Gronostajski, and Daniel L. Kilpatrick. "BDNF activates an NFI-dependent neurodevelopmental timing program by sequestering NFATc4." Molecular Biology of the Cell 29, no. 8 (April 15, 2018): 975–87. http://dx.doi.org/10.1091/mbc.e16-08-0595.

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How intrinsic and extrinsic signals are coordinated to regulate synaptic maturation and its timing is an important question for neurodevelopment and its disorders. We investigated the influence of the neurotrophin BDNF on the developmental timing of a dendrite/synapse-related gene program controlled by nuclear factor I (NFI) in maturing cerebellar granule neurons (CGNs). BDNF accelerated the onset of NFI-regulated late-gene expression and NFI temporal occupancy in CGN cultures in a MEK5/ERK5-dependent manner. BDNF and NFI occupancy were mutually regulating, with BDNF enhancing the temporal binding of NFI to the Bdnf4 promoter itself. Moreover, BDNF induced phosphorylation and accelerated the departure of the trans-repressor NFATc4 from NFI late-gene promoters, including Bdnf4, which is permissive for NFI binding. BDNF dismissal of NFATc4 from late genes was linked to MEK5/ERK5-dependent sequestration of NFATc4 in the cis–Golgi, an event mirrored in CGNs developing in vivo. These studies reveal an expanded autoregulatory gene network for NFI temporal occupancy involving BDNF and NFATc4 extranuclear sequestration. Based on these and earlier findings, NFATc4 integrates intrinsic developmental signaling from membrane potential/calcineurin and autocrine/paracrine BDNF/TrkB to control initiation of NFI occupancy in maturing CGNs. We also identify a local Bdnf/Etv1 gene circuit within the larger NFI autoregulatory network.
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Efffendy, Elmeida, Muhammad Sjahrir, and Nurul Utami. "The Relationship between Brain-derived Neurotrophic Factor’s Serum Level and Hospital Anxiety and Depression Scale-depression in Patients with Psoriasis Vulgaris." Open Access Macedonian Journal of Medical Sciences 9, T3 (May 20, 2021): 164–67. http://dx.doi.org/10.3889/oamjms.2021.6290.

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BACKGROUND: Psoriasis vulgaris is a chronic inflammatory skin disorder that can lead to depression. The involvement of the nervous system in psoriasis was proved by the influence of brain-derived neurotrophic factor (BDNF) in regulating corneocyte homeostasis. Low level of BDNF in patients with psoriasis result in transit amplifying subpopulation of basal keratinocytes not performing their function as inhibitors of keratinocyte proliferation, resulting in acceleration of keratinocyte proliferation. In depressed patients, it is known that levels of BDNF in the serum and hippocampus are low. BDNF level imbalance potentially affects the severity of psoriasis and depression. METHODS: This is an analytical cross-sectional study. The measurement of BDNFs serum level was carried out in the Medan Private Laboratory using a human BDNF (R and D®, USA) kit using the ELISA method. We use hospital anxiety and depression scale (HADS-D) questionnaire to assess depression symptoms. RESULTS: The results of the Spearman correlation test for BDNFs serum level and HADS-D showed p < 0.05, it can be concluded that there is a correlation between BDNFs serum level and HADS-D. The strength of the relationship between HADS-D and BDNFs serum level is −0.537 that shows moderate correlation (r = 0.4 −<0.6). Relationship between HADS-D and BDNFs serum level is −0.537 that shows moderate correlation (r = 0.4 −<0.6). CONCLUSION: This study shows a moderate negative relationship between BDNFs serum level and the degree of symptoms of depression, which the lower level of BDNFs serum will increase the degree of depression symptoms.
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Jo, Danbi, Yujeong Son, Gwangho Yoon, Juhyun Song, and Oh Yoen Kim. "Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning." Journal of Clinical Medicine 10, no. 1 (December 26, 2020): 56. http://dx.doi.org/10.3390/jcm10010056.

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Obesity, characterized by excessive fat mass, has been emerging as a major global epidemic and contributes to the increased risk of morbidity around the world. Thus, the necessity to find effective therapy and specific regulatory mechanisms is increasing for controlling obesity. Lately, many researchers have been interested in the linkage between obesity and adipokines/myokines, particularly adiponectin and brain-derived neurotrophic factor (BDNF). However, the role of adiponectin and BDNF in adiposity has not been clearly defined yet. We examined the association of adiposity with adiponectin and BDNF through human study (observational study) with Korean women and in vitro experiments. In the human study, we found a negative relationship between adiposity and circulating adiponectins but irregular patterns in the relationship between adiposity and circulating BDNFs. In the in vitro study using 3T3-L1 adipocytes, adiponectin treatment strongly promoted adipocyte differentiation and the fat browning process, whereas BDNF treatment attenuated adipocyte differentiation and the fat browning process in differentiated adipocytes. Our results demonstrate that adiponectin and BDNF play an important role in regulating fat mass and the expression of fat-browning markers in different ways, and also suggest that circulating adiponectin may be used as an important monitoring index for obesity status.
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Baglan Yentur, S., Z. Ercan, G. Deniz, A. Karatas, M. Gur, G. Alkan, and S. S. Koca. "POS0576 EFFECTS OF ACUTE EXERCISE ON SERUM BDNF LEVEL IN PATIENTS WITH RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 522.1–522. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3768.

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Background:Brain derived neurotrophic factor (BDNF) is a neurotrofic factor that may show healing, survival-promoting and protective effects on neurons in central and peripheral nervous system. The effect of physical exercise on serum BDNF is unclear. Also, BDNF level was found significantly lower in rheumatoid Arthritis (RA) patients with depression.Objectives:Aim of this study is to investigate the variation of BDNF levels following acute exercise and potential correlation between BDNF levels and depression.Methods:This study included 44 RA patients and 44 age and sex matched healthy controls (HC). Aerobic exercise was performed to all participants for a single session. The intervention was performed on a treadmill and included 5 minutes of warm-up, 20 minutes of walking exercise reaching at 60- 80% of Maximal heart rate and 5 minutes of cool-down. Depression and anxiety levels were evaluated with Beck Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS). Blood samples from all subjects were taken and centrifuged before and immediately after the exercise intervention.Results:Serum BDNF levels (both baseline and post-exercise) were similar in the RA and HC group (Table 1). Although after aerobic exercise serum BDNF levels were significantly decreased in both RA and HC groups (Wilcoxon Rank P < 0.05) ΔBDNF levels was significantly higher in the RA group than HC group. Serum BDNF level was increased in 30.2% of healthy subjects and 4.5% of RA patients (P = 0.002). On the other hand, BDI, HADS depression and HADS anxiety indices were correlated significantly with ΔBDNF levels in the RA group (p<0.05) but not in HC group.Conclusion:A single bout of exercise may be effective on serum BDNF levels in patients with RA and healthy subjects. However, psychological comorbidities affect the amelioration of BDNF level, in RA. The long-term effect of alterations on BDF level is candidate to evaluate by prospective studies.Table 1.Clinical and laboratory characteristics in the study groupsRA (n=44)HC (n=44)PMean age, years46.8±10.343.4±6.40.071*Females, n (%)32 (72.7)31 (70.5)0.813**Active smokers, n (%)12 (27.3)10 (22.7)0.622**BMI, kg/m226.8±4.625.6±2.40.127*HADS Depression10.2±3.92.2±2.1<0.001*HADS Anxiety10.4±4.12.4±2.1<0.001*BDI17.9±8.13.7±4.1<0.001*BDNF (baseline), pg/ml798.9±381.1688.7±469.90.069***BDNF (post-exercise), pg/ml469.5±193.5509.9±380.40.593***ΔBDNF, pg/ml329.5±258.4211.1±302.60.047***BDNF increased, n (%)2 (4.5)13 (30.2)0.002**RA; rheumatoid arthritis, HC; healthy control, BMI; body mass index, HADS; Hospital Anxiety and Depression Scale, BDI; Beck Depression Inventory, BDNF; brain derived neurotrophic factor*Student’s t test, **Chi square test and ***Mann Whitney U testDisclosure of Interests:None declared
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McAllister, A. Kimberley. "BDNF." Current Biology 12, no. 9 (April 2002): R310. http://dx.doi.org/10.1016/s0960-9822(02)00825-4.

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Wong, Yu-Hui, Chia-Ming Lee, Wenjun Xie, Bianxiao Cui, and Mu-ming Poo. "Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin." Proceedings of the National Academy of Sciences 112, no. 32 (July 27, 2015): E4475—E4484. http://dx.doi.org/10.1073/pnas.1511830112.

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Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation.
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Пальцын, А. А. "Brain-derived neurotrophic factor (BDNF)." Nauchno-prakticheskii zhurnal «Patogenez», no. 3() (December 12, 2019): 83–88. http://dx.doi.org/10.25557/2310-0435.2019.03.83-88.

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Сегодня нейротрофический фактор мозга (BDNF) - вещество очень популярное. Большой интерес к белку объясняется его участием в важнейших для жизни и здоровья процессах: нервной регуляции, углеводном и липидном обмене, адаптации к физическим нагрузкам. Вещество участвует в регуляции эффективности профилактических и лечебных процедур, эмоционального состояния, стрессоустойчивости, нейропластичности, нейрогенеза. BDNF - главный регулятор действия самого универсального и, часто, самого эффективного лечебного средства - физических нагрузок. Следовательно, он становится веществом первостепенного значения в одной из самых актуальных проблем современной медицины - профилактике и лечении гипертонической болезни. Кроме гипотензивного действия, доказана эффективность BDNF при обусловленных гипертонией когнитивных нарушениях, шизофрении, дефектах памяти, эмоциональных расстройствах. Today, the brain-derived neurotrophic factor (BDNF) is a very popular substance. The high interest to this protein is due to its participation in key processes for life and health, including nervous regulation, carbohydrate and lipid metabolism, and exercise capacity. BDNF regulates preventive and therapeutic efficacy of exercise, emotional state, stress resistance, neuroplasticity, and neurogenesis. BDNF determines the action of the most universal and often the most effective therapeutic means, physical exercise. Therefore, BDNF appears to be the substance of primary importance for a burning issue of current medicine, prevention and treatment of hypertension. In addition to its hypotensive effect, BDNF has proved to be beneficial in hypertension-induced cognitive decline, schizophrenia, memory impairment, and emotional disorders.
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Chu, Pengcheng, Wei Guo, He You, and Bai Lu. "Regulation of Satiety by Bdnf-e2-Expressing Neurons through TrkB Activation in Ventromedial Hypothalamus." Biomolecules 13, no. 5 (May 11, 2023): 822. http://dx.doi.org/10.3390/biom13050822.

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The transcripts for Bdnf (brain-derived neurotrophic factor), driven by different promoters, are expressed in different brain regions to control different body functions. Specific promoter(s) that regulates energy balance remain unclear. We show that disruption of Bdnf promoters I and II but not IV and VI in mice (Bdnf-e1−/−, Bdnf-e2−/−) results in obesity. Whereas Bdnf-e1−/− exhibited impaired thermogenesis, Bdnf-e2−/− showed hyperphagia and reduced satiety before the onset of obesity. The Bdnf-e2 transcripts were primarily expressed in ventromedial hypothalamus (VMH), a nucleus known to regulate satiety. Re-expressing Bdnf-e2 transcript in VMH or chemogenetic activation of VMH neurons rescued the hyperphagia and obesity of Bdnf-e2−/− mice. Deletion of BDNF receptor TrkB in VMH neurons in wildtype mice resulted in hyperphagia and obesity, and infusion of TrkB agonistic antibody into VMH of Bdnf-e2−/− mice alleviated these phenotypes. Thus, Bdnf-e2-transcripts in VMH neurons play a key role in regulating energy intake and satiety through TrkB pathway.
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McAllan, Liam, Kristen R. Maynard, Alisha S. Kardian, Amanda S. Stayton, Shelby L. Fox, Erin J. Stephenson, Clint E. Kinney, et al. "Disruption of brain-derived neurotrophic factor production from individual promoters generates distinct body composition phenotypes in mice." American Journal of Physiology-Endocrinology and Metabolism 315, no. 6 (December 1, 2018): E1168—E1184. http://dx.doi.org/10.1152/ajpendo.00205.2018.

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Brain-derived neurotrophic factor (BDNF) is a key neuropeptide in the central regulation of energy balance. The Bdnf gene contains nine promoters, each producing specific mRNA transcripts that encode a common protein. We sought to assess the phenotypic outcomes of disrupting BDNF production from individual Bdnf promoters. Mice with an intact coding region but selective disruption of BDNF production from Bdnf promoters I, II, IV, or VI (Bdnf-e1−/−, -e2−/−, -e4−/−, and -e6−/−) were created by inserting an enhanced green fluorescent protein-STOP cassette upstream of the targeted promoter splice donor site. Body composition was measured by MRI weekly from age 4 to 22 wk. Energy expenditure was measured by indirect calorimetry at 18 wk. Food intake was measured in Bdnf-e1−/− and Bdnf-e2−/− mice, and pair feeding was conducted. Weight gain, lean mass, fat mass, and percent fat of Bdnf-e1−/− and Bdnf-e2−/− mice (both sexes) were significantly increased compared with wild-type littermates. For Bdnf-e4−/− and Bdnf-e6−/− mice, obesity was not observed with either chow or high-fat diet. Food intake was increased in Bdnf-e1−/− and Bdnf-e2−/− mice, and pair feeding prevented obesity. Mutant and wild-type littermates for each strain (both sexes) had similar total energy expenditure after adjustment for body composition. These findings suggest that the obesity phenotype observed in Bdnf-e1−/− and Bdnf-e2−/− mice is attributable to hyperphagia and not altered energy expenditure. Our findings show that disruption of BDNF from specific promoters leads to distinct body composition effects, with disruption from promoters I or II, but not IV or VI, inducing obesity.
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Dissertations / Theses on the topic "BDNF"

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Zhu, Wenjun. "The role of brain derived neurotrophic factor in multiple sclerosis and the role of fractalkine in multiple sclerosis induced neuropathic pain." Journal of Neuroscience Methods, 2010. http://hdl.handle.net/1993/16675.

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Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease, characterised by demyelination in the central nervous system (CNS). The exact pathophysiology of MS is still unknown but it is believed to be associated with infiltration of T cells and activation of microglia that result in myelin damage leading to neurological deficits including neuropathic pain. Current treatment strategies such as glatiramer acetate have recognized the importance of BDNF in myelin repair. In addition, the proposed role of the chemokine CX3CL1 and its receptor CX3CR1 in the control of microglia activation and leukocyte infiltration place this chemokine in an important position in regulation of MS-induced neuropathic pain. In this research study, the experimental autoimmune encephalomyelitis (EAE) rat model of MS was used to examine the role of BDNF in myelin repair as well as CX3CL1’s role in neuropathic pain. Methods: A total of 66 adult female Lewis rats are divided into 3 experimental groups: naïve control, active control and active EAE. Naïve control animals do not receive any injections. Active control animals receive 2 intraperitoneal injections of pertussis toxin and injections of Freund’s adjuvant and Mycobacterium Tuberculosis. Active EAE animals receive the same regimen administered to active controls plus full inoculation with fatty acid and Guinea pig myelin basic protein. Expressions of BDNF, CX3CL1 and CX3CR1 in a time dependent mansion (day 0, 3, 6, 9, 12 &15) were examined using immunohistochemistry (IHC), ELISA, Western blot, RT-PCR and real time-PCR. Results: There was a significant increase in BDNF, CX3XL1 and CX3CR1 expression of protein and mRNA in DRG at day 12 after induction of MS. The neurons and glial cells were identified to express BNDF, CX3XL1 and CX3CR1 in the spinal cord of EAE animal. Conclusion: The antigenic-induced expression of BDNF within the DRG may represent a key element involved in facilitating central myelin repair. In addition, the chemokine CX3CL1 and its receptor CX3CR1 represent key mediators involved in the development of MS-induced pain. Keywords: Multiple sclerosis, MS, experimental autoimmune encephalomyelitis, EAE, CX3CL1, CX3CR1, neuropathic pain, myelin repair
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Zuena, Anna Rita. "Lo Stress Prenatale nel ratto come modello di depressione: accertamento della validità predittiva con l'imipramina e studio della neurogenesi dopo trattamento con una nuova molecola, l'agomelatina (S-20098)." Doctoral thesis, La Sapienza, 2005. http://hdl.handle.net/11573/917224.

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Hartmann, Matthias. "Die Freisetzung von BDNF an glutamatergen Synapsen und die Stimulation der Filopodienbildung durch den trunkierten BDNF-Rezeptor TrkB.T1." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965079686.

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Huie, John Russell. "The role of BDNF in spinal learning." [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-2824.

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Pichler, Bruno. "Charakterisierung BDNF-induzierter Calciumtransienten in kultivierten Astrozyten." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=98029391X.

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Fayard, Bérengère. "Studies on the binding properties and functional activities of the precursor of BDNF, proBDNF, and of engineered BDNF mutants /." [S.l.] : [s.n.], 2004. http://www.zb.unibe.ch/download/eldiss/04fayard_b.pdf.

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Béjot, Yannick. "Infarctus cérébral et plasticité : focus sur le BDNF." Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00939908.

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La récupération fonctionnelle des patients victimes d'un accident vasculaire cérébral (AVC) ischémique est largement sous-tendue par les propriétés plastiques du cerveau et plus précisément par sa capacité à remodeler les réseaux de neurones épargnés par l'infarctus. Les études réalisées sur différents modèles animaux d'infarctus cérébral s'accordent à montrer que ces changements plastiques sont induits par le BDNF (Brain-Derived Neurotrophic Factor). Aussi, augmenter les taux cérébraux de BDNF est considéré comme une stratégie thérapeutique prometteuse de réduction des déficiences post-AVC. Dans ce contexte, notre travail avait 2 objectifs : 1) chez le rat, identifier les cellules impliquées dans la surproduction de BDNF et évaluer la pertinence de la mesure des taux circulants de BDNF pour estimer les taux de BDNF présents dans le cerveau, 2) chez le patient victime d'un infarctus cérébral, étudier l'efficacité de la fluoxétine sur la récupération motrice à 3 mois, la fluoxétine étant un inhibiteur spécifique de la recapture de la sérotonine commercialisé comme antidépresseur et capable non seulement d'augmenter la production cérébrale de BDNF mais aussi de stimuler la plasticité post-lésionnelle.Les études précliniques ont été réalisées chez le rat soumis à l'embolisation unilatérale du cerveau par un nombre variable de microsphères (en carbone et calibrées à 50 µm) afin de reproduire le large panel de souffrance cérébrale rencontré en clinique. Le BDNF a été mesuré dans le cerveau et dans le sang (plasma et sérum par technique ELISA) avant et après (4, 24h et 8j) embolisation. Nos résultats montrent :- que la production de BDNF est plus intense et plus durable dans l'hémisphère embolisé que dans l'hémisphère non embolisé et que cette production est indépendante du degré d'embolisation, marqueur indirect de la souffrance cérébrale. - que les cellules non-neuronales deviennent une source non négligeable de BDNF en cas d'ischémie, notamment les cellules endothéliales et microgliales avant 24h et les astrocytes au temps 8j.- que les taux circulants et cérébraux de BDNF ne sont pas corrélés mais qu'il existe une corrélation entre le BDNF plasmatique mesuré au temps 4h et le degré d'embolisation.L'étude clinique correspond à un essai randomisé contrôlé en double aveugle comparant la fluoxétine (20mg/j, voie orale, pendant 3 mois et débutée entre 5 et 10j après les premiers symptômes) au placebo chez des patients présentant un déficit moteur modéré à sévère sur l'échelle motrice de Fugl-Meyer (n=59 dans chaque groupe). Nos résultats montrent que l'amélioration de la fonction motrice est meilleure sous fluoxétine que placebo. En conclusion, notre travail montre l'intérêt des médicaments capables d'augmenter le BDNF et la plasticité post-lésionnelle pour améliorer le pronostic clinique de l'AVC et identifie pour la première fois les cellules endothéliales cérébrales comme une cible potentielle de ces médicaments. Il remet également en cause l'idée largement répandue selon laquelle les taux circulants de BDNF varient dans le même sens que les taux cérébraux.
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Kerr, Bradley James. "Novel modulators of central sensitization : BDNF and galanin." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246735.

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Pedard, Martin. "Endothélium, inflammation et cognition : focus sur le BDNF." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCI008/document.

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Le BDNF (brain-derived neurotrophic factor) a été découvert dans le cerveau et est largement impliqué dans la neuroplasticité, la mémoire et la cognition via l’activation des récepteurs TrkB (tropomyosin receptor kinase B) neuronaux. Nous avons récemment montré que le système cardiovasculaire contenait autant de BDNF que le cerveau et que le BDNF exogène était capable d’induire une relaxation vasculaire dépendante de l’endothélium. D’autres études ont suggéré que l’activation des récepteurs TrkB endothéliaux par le BDNF était impliquée dans les processus athérosclérotiques. Notre laboratoire soupçonne une interaction étroite entre NO et BDNF endothélial et a même envisagé la possibilité d’une implication du BDNF secrété par l’endothélium des microvaisseaux cérébraux dans la cognition. Les patients souffrant de polyarthrite rhumatoïde (PR), une maladie inflammatoire d’origine auto-immune, sont à risque cardiovasculaire et présentent une altération de la cognition avec notamment un risque plus élevé de dépression. Etonnamment, l’effet de la PR sur le BDNF est peu documenté. Les seules études disponibles rapportent une élévation du BDNF dans le sang et le liquide synovial en cas de PR. Notre hypothèse est qu’une réduction de l’expression endothéliale du BDNF pourrait contribuer au risque cardiovasculaire et au déficit cognitif associés à la PR. Ainsi, dans notre travail, nous avons étudié le BDNF vasculaire et cérébral et son récepteur TrkB sur le modèle rat d’arthrite induite à l’adjuvant.Nos principaux résultats montrent que l’arthrite conduit à 1) une réduction des taux aortiques de BDNF indépendamment de la sévérité des symptômes inflammatoires mais dépendante de la fonction endothéliale, 2) une diminution des taux cérébraux en BDNF indépendamment de la sévérité des symptômes inflammatoires mais en lien avec la fonction endothéliale, 3) une diminution de l’expression du BDNF et de son récepteur TrkB activé au niveau tant neuronal qu’endothélial dans les régions cérébrales impliquées dans la cognition, 4) une corrélation positive entre l’expression du BDNF par l’endothélium vasculaire et l’expression neuronale des TrkB activés, 5) une absence de corrélation entre les taux sériques de BDNF et ses taux cérébraux ou vasculaires mais en revanche l’existence d’une corrélation positive entre les taux sériques de BDNF et l’inflammation qu’elle soit clinique ou biologique.L’ensemble de ces données est en faveur de l’hypothèse selon laquelle le BDNF endothélial pourrait être impliqué dans le risque athérosclérotique et le déficit cognitif associé à l’arthrite. L’inflammation doit être considérée comme un facteur confondant lorsque les taux circulants de BDNF sont utilisés comme un reflet des taux présents dans le cerveau
BDNF (brain-derived neurotrophic factor) has been discovered in the brain and is widely implicated in neuroplasticity, memory and cognition through the activation of neuronal TrkB (tropomyosin receptor kinase B) receptors. We have recently shown that the cardiovascular system contained as much BDNF as the brain and that exogenous BDNF was able to induce endothelium-dependent vascular relaxation. Other studies have suggested that activation of endothelial TrkB receptors by BDNF is involved in atherosclerotic processes. Our laboratory suspects a close interaction between endothelial NO and BDNF and has even considered the possibility of involvement of BDNF secreted by cerebral microvessel endothelium in cognition. Patients suffering from rheumatoid arthritis (RA), an inflammatory disease of autoimmune origin, are at risk of cardiovascular disease and have an impairment of cognition, including a higher risk of depression. Surprisingly, the effect of RA on BDNF is poorly documented. The only available studies report an increase of BDNF in the blood and synovial fluid in RA. Our hypothesis is that a reduction in endothelial expression of BDNF may contribute to the cardiovascular risk and cognitive deficit associated with RA. Thus, in our work, we studied vascular and cerebral BDNF and its TrkB receptor on the rat model of adjuvant-induced arthritis.Our main findings show that arthritis leads to 1) a decrease in BDNF levels in aortas independently of the severity of inflammatory symptoms but dependent on endothelial function, 2) a decrease in brain BDNF levels independent of the severity of inflammatory symptoms, but link with endothelial function, 3) a decreased expression of BDNF and its activated TrkB receptor at both neuronal and endothelial levels in the brain regions involved in cognition, 4) a positive correlation between endothelial expression of BDNF and neuronal expression of activated TrkB, 5) a lack of correlation between serum BDNF levels and its cerebral or vascular levels, but on the other hand the existence of a positive correlation between serum BDNF levels and inflammation, whether clinical or biological.All of these data support the hypothesis that endothelial BDNF may be involved in atherosclerotic risk and cognitive impairment associated with arthritis. Inflammation should be considered as a confounding factor when circulating levels of BDNF are used as a reflection of levels present in the brain
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Quirié, Aurore. "BDNF cérébral et cardiovasculaire : effet de l'activité physique." Thesis, Dijon, 2013. http://www.theses.fr/2013DIJOS073.

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La pratique régulière d’une activité physique (AP) est un important message de santé publique tant pour ces bénéfices cardiovasculaires que cérébraux. Par ailleurs, la rééducation par le mouvement et notamment l’exercice sur tapis roulant est de plus en plus utilisée pour accélérer la récupération après un accident vasculaire cérébral (AVC). Il est admis que l’AP impacte positivement le fonctionnement cérébral via l’augmentation des taux de BDNF (brain-derived neurotrophic factor) dans le cerveau et que son bénéfice cardiovasculaire est à relier à une modification du phénotype endothélial. Dans un premier temps, nous avons mis au point le dosage par Western blotting du proBDNF et du BDNF mature (BDNFm) ainsi que les techniques immunohistochimiques permettant de localiser le BDNF à l’étage cellulaire. Dans un second temps, nous avons comparé l’effet d’une AP (tapis roulant, 30min/j, 18m/min, 7 jours consécutifs) sur le métabolisme et la localisation du BDNF chez des rats sains versus soumis à une ischémie cérébrale focale. Dans un dernier temps, nous nous sommes intéressés à l’expression du BDNF cardiovasculaire chez des rats normo- ou hypertendus, sédentaires ou soumis au modèle d’AP précédent. Les principaux résultats montrent que 1) l’AP augmente les taux de proBDNF et de BDNFm aussi bien dans le cerveau (neurones et cellules endothéliales) que dans le système cardiovasculaire (endothélium vasculaire et cardiaque), 2) l’ischémie cérébrale n’entrave pas les effets cérébraux de l’AP sur le BDNFm, 3) l’expression endothéliale (cœur, aorte, artère coronaire) du BDNF est moindre en cas d’hypertension, 4) la synthèse et la sécrétion de BDNF par des cellules endothéliales en culture augmentent lorsque les cellules sont soumises à des contraintes de cisaillement, 5) le BDNF exerce un effet vasodilatateur sur le modèle d’aorte isolée. En conclusion, notre travail montre qu’il est possible de sélectionner, chez des rats sains, des protocoles d’AP capables d’augmenter la neuroplasticité dépendante du BDNF chez des rats ischémiés. Il identifie également le BDNF d’origine endothéliale comme un marqueur potentiel de la fonction endothéliale et un acteur jusque-là ignoré des changements neuroplastiques induits par l’AP
The regular practice of physical activity is an important message for public health as it has both cardiovascular and brain benefits. Furthermore, rehabilitation programs involving movement especially the treadmill exercise are being used increasingly to accelerate post stroke recovery. It is recognised that the physical activity has a positive impact on brain function through increased levels of BDNF (brain-derived neurotrophic factor) in the brain and that its cardiovascular benefit is connected to a change in endothelial phenotype. As a first step, we developped the dosage by Western blotting of proBDNF and mature BDNF (mBDNF) and the immunohistochemical techniques in order to localise BDNF in the cell floor. As a second step, we compared the effect of physical activity (treadmill exercise, 30min/d, 18m/min, 7 consecutive days) on the metabolism and localisation of BDNF in healthy rats versus rats subjected to focal cerebral ischemia. As a final step, we looked into the expression of cardiovascular BDNF in normotensive or hypertensive rats, sedentary or subjected to the same physical activity. The main results show that 1) physical activity increases the levels of proBDNF and mBDNF in both brain (neurons and endothelial cells) and cardiovascular system (heart and vascular endothelium), 2) cerebral ischemia does not change the cerebral effects of physical activity on mBDNF, 3) endothelial expression (heart, aorta, coronary artery) of BDNF is reduced in the presence of hypertension, 4) the synthesis and secretion of BDNF by endothelial cells in culture increase when the cells are subjected to shear stress, 5) BDNF has a vasodilatator effect on the isolated aorta model. In conclusion, our work shows that it is possible to select, in healthy rats, protocols of physical activity that are able to increase the BDNF-dependent neuroplasticity in ischemic rats. It also identifies endothelial BDNF as a potential marker of endothelial function as well as a potential contributor of physical activity-induced neuroplasticity
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Books on the topic "BDNF"

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Duarte, Carlos B., and Enrico Tongiorgi, eds. Brain-Derived Neurotrophic Factor (BDNF). New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8970-6.

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Madra, Moneek. Interactions between the BDNF (Val66Met) variant and stress as a model of susceptibility to Anorexia Nervosa. [New York, N.Y.?]: [publisher not identified], 2015.

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Duarte, Carlos B., and Enrico Tongiorgi. Brain-Derived Neurotrophic Factor (BDNF). Springer New York, 2019.

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Duman, Ronald S. Neurotrophic Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.
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Poretti, Andrea, and Michael V. Johnston. Genetic Disorders and Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0110.

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A variety of monogenic and polygenic genetic disorders have been linked to stroke, making it important for the clinician to keep up with the new discoveries and the potential to provide new gene-based therapies. Hematologic disorders such as sickle cell disease and thrombophilia due to mutations in prothrombin, factor V Leiden, and homocysteine metabolism are fairly well known, but mutations in mitochondrial metabolism and matrix metalloproteinases are less recognized. In addition, results of genome-wide association studies (GWAS) in stroke populations are revealing mutations that could predispose to stroke in specific ethnic populations. These studies are also revealing some crossover in mutations between stroke and familial hemiplegic migraine as well as mutations in growth factors such as brain derived neurotrophic factor (BDNF) that appear to influence the recovery from stroke by altering cortical plasticity.
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Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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Maternal Exercise during Pregnancy Increases BDNF Levels and Cell Numbers in the Hippocampal Formation but Not in the Cerebral Cortex of Adult Rat Offspring. Plos one, 2016.

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Lempert, Tammy. Guess What BDF Means? Independently Published, 2022.

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Lex, Maja, and Graziela Padilla. Elementarer Tanz, in 3 Bdn. Noetzel, 1988.

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Dostoyevsky, Fyodor Mikhaylovich. Die Dämonen: In 2 Bdn. Aufbau-Verlag, 1994.

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Book chapters on the topic "BDNF"

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Tyrer, Peter J., Mark Slifstein, Joris C. Verster, Kim Fromme, Amee B. Patel, Britta Hahn, Christer Allgulander, et al. "BDNF." In Encyclopedia of Psychopharmacology, 201. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3114.

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Hill, Keith, Tom Baranowski, Walter Schmidt, Nicole Prommer, Michel Audran, Philippe Connes, Ramiro L. Gutiérrez, et al. "BDNF." In Encyclopedia of Exercise Medicine in Health and Disease, 116. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2140.

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Gomes, João R., Andrea Lobo, Carlos B. Duarte, and Mário Grãos. "BDNF-Induced Intracellular Signaling." In Brain-Derived Neurotrophic Factor (BDNF), 161–83. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_6.

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Vatanashevanopakorn, Chinnavuth, Amit Grover, Arup R. Nath, Kevin Clark, Paul Sopp, Claus Nerlov, and Liliana Minichiello. "Studying BDNF/TrkB Signaling: Transcriptome Analysis from a Limited Number of Purified Adult or Aged Murine Brain Neurons." In Brain-Derived Neurotrophic Factor (BDNF), 55–76. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_3.

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Nath, Arup R., Roy Drissen, Fei Guo, Claus Nerlov, and Liliana Minichiello. "Studying BDNF/TrkB Signaling: High-Throughput Microfluidic Gene Expression Analysis from Rare or Limited Samples of Adult and Aged Central Neurons." In Brain-Derived Neurotrophic Factor (BDNF), 77–86. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_4.

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Salio, Chiara, and Adalberto Merighi. "Ultrastructural Localization of BDNF and trkB Receptors." In Brain-Derived Neurotrophic Factor (BDNF), 133–48. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_5.

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Panja, Debabrata, and Clive R. Bramham. "BDNF Function in Long-Term Synaptic Plasticity in the Dentate Gyrus In Vivo: Methods for Local Drug Delivery and Biochemical Analysis of Translation." In Brain-Derived Neurotrophic Factor (BDNF), 241–56. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7657_2017_7.

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Jaanson, Kaur, Angela Pärn, and Tõnis Timmusk. "Usage of Bacterial Artificial Chromosomes for Studying BDNF Gene Regulation in Primary Cultures of Cortical Neurons and Astrocytes." In Brain-Derived Neurotrophic Factor (BDNF), 13–25. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/7657_2018_10.

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Vermehren-Schmaedick, Anke, Thomas Jacob, and Tania Q. Vu. "Methodology for Detecting and Tracking Brain-Derived Neurotrophic Factor Complexes in Neurons Using Single Quantum Dots." In Brain-Derived Neurotrophic Factor (BDNF), 105–18. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/7657_2018_11.

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Hall, Charles E., James O. McNamara, and Ryohei Yasuda. "Analysis of TrkB Receptor Activity Using FRET Sensors." In Brain-Derived Neurotrophic Factor (BDNF), 149–57. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/7657_2018_12.

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Conference papers on the topic "BDNF"

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Alomari, Mahmoud, and Omar F. Khabour. "Stepwise Relationship of Exercise Frequency with Serum BDNF Level among Adolescents." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0148.

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Introduction: Regular participation in exercise in adolescents is associated with numerous health benefits, including improved CV, metabolic, muscular, respiratory, immune, cognitive, and neurohormonal functions. Brain-derived neutrophic factor (BDNF) is essential for several body functions, particularly the neural and cognitive functions. However, the dose-effect of exercise participation on BDNF is not fully understood among adolescents. The current study examined the relationship of serum BDNF level with moderate/vigorous exercise frequency in 703 adolescents aged 13-17 years old. Methodology: ELISA was used to evaluate serum BDNF. Additionally, the SALSA questionnaire was used to obtain the weekly frequency of moderate/vigorous exercise. Results: The ANOVA revealed differences (p=0.001) in BDNF level according to running frequency. Subsequent posthoc analysis showed that BDNF was greater (p<0.05) in adolescents participating three, four, five, six, and seven versus no and one day of exercise. Furthermore, no differences (p>0.05) were found in BDNF between exercising three, four, five, six, and seven days/week. Conclusion: The current data revealed stepwise differences in BDNF between running frequencies, peaking at five days/week. These differences in BDNF seems to plateau when participating more than three days/week. The results confirm the importance of exercise for brain health and are consistent with the current recommendations for moderate/vigorous exercise frequency.
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Dragunas, Guilherme, Manon Woest, Susan Nijboer, Sophie Bos, Corneel Vermeulen, Ben Ditz, Judith Vonk, et al. "BDNF-TrkB signaling mediates cholinergic neuroplasticity in asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa4957.

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Gabrielpillai, J., H. Petzold, C. Geissler, T. Stöver, and M. Diensthuber. "BDNF limits cisplatin-induced toxicity to auditory neurons." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686372.

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Shi, Aike. "Effects of BDNF and ANK3 in bipolar disorder." In 4TH INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2021). AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0094319.

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Sorokina, Elena, Zhanna Semenova, Valery Ivanovich Lukianov, Olga Karaseva, Sofya A. Afanasieva, Valentin Reutov, Leonid Michailovich Roshal, and Vsevolod Grigorievich Pinelis. "BIOCHEMICAL PREDICTORS OF EARLY AND LONG-TERM OUTCOMES OF TRAUMATIC BRAIN INJURY IN CHILDREN." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.24.

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In children with mild and severe traumatic brain injury (TBI), the role of various damage/repair neuromarkers in the outcomes of trauma was studied. It has been shown that in the first days after TBI with adverse outcomes, there was a significant increase in NSE, S100b, NO products and a decrease in the content of BDNF and autoantibodies to NMDA (NR2) glutamate receptors (Glu) in the blood serum. After 6 months with unfavorable outcomes, there was an increase in aAb to S100b and a decrease in BDNF.
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Belousova, N. P. "Interethnic Analysis Of Bdnf Level Quantitative Indicator In Youths." In RPTSS 2018 - International Conference on Research Paradigms Transformation in Social Sciences. Cognitive-Crcs, 2018. http://dx.doi.org/10.15405/epsbs.2018.12.22.

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Gabrielpillai, J., H. Petzold, C. Geissler, T. Stöver, and M. Diensthuber. "BDNF limitiert die Cisplatin-induzierte Toxizität auf auditorische Neuronen." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686148.

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Dong, Yue, Kunjie Liu, and Yushi Wu. "The Function of BDNF and Treatment in Neurological Disorder." In International Conference on Health Big Data and Intelligent Healthcare. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011269100003438.

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Adekunle, A. N., M. Gabani, and I. Brimah. "Association of Serum BDNF with Obstructive Sleep Apnea Severity." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3660.

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Flores, Krisstopher Richard, Fausta Viccaro, Mauro Aquilini, Francesco Ronchetti, Stefania Scarpino, Arianna Di Napoli, Giorgia Scafetta, Paolo Palange, and Alberto Ricci. "Serum and mucosal brain derived neurotrophic factor (BDNF) in severe obstructive sleep apnea syndrome (OSAS). Effects of CPAP treatment on BDNF serum levels." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4177.

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Reports on the topic "BDNF"

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Hicks, Ramona R. Brain-Derived Neurotrophic Factor (BDNF) and Traumatic Brain Injury (Head and Spinal). Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada375796.

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Alves-Borba, Laryssa, Verónica Espinosa-Fernández, Ania Canseco Rodriguez, and Ana María Sánchez-Pérez. ABA Supplementation Rescues IRS2 and BDNF mRNA Expression in a Triple-Transgenic Mice Model of Alzheimer’s Disease. Universitat Jaume I, 2023. http://dx.doi.org/10.6035/uji_b201801.

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A.J. SMITH. ABSTRACTION OF BDCF DISTRIBUTIONS FOR IRRIGATION PERIODS. Office of Scientific and Technical Information (OSTI), December 2000. http://dx.doi.org/10.2172/861089.

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Meiri, Noam, Michael D. Denbow, and Cynthia J. Denbow. Epigenetic Adaptation: The Regulatory Mechanisms of Hypothalamic Plasticity that Determine Stress-Response Set Point. United States Department of Agriculture, November 2013. http://dx.doi.org/10.32747/2013.7593396.bard.

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Our hypothesis was that postnatal stress exposure or sensory input alters brain activity, which induces acetylation and/or methylation on lysine residues of histone 3 and alters methylation levels in the promoter regions of stress-related genes, ultimately resulting in long-lasting changes in the stress-response set point. Therefore, the objectives of the proposal were: 1. To identify the levels of total histone 3 acetylation and different levels of methylation on lysine 9 and/or 14 during both heat and feed stress and challenge. 2. To evaluate the methylation and acetylation levels of histone 3 lysine 9 and/or 14 at the Bdnfpromoter during both heat and feed stress and challenge. 3. To evaluate the levels of the relevant methyltransferases and transmethylases during infliction of stress. 4. To identify the specific localization of the cells which respond to both specific histone modification and the enzyme involved by applying each of the stressors in the hypothalamus. 5. To evaluate the physiological effects of antisense knockdown of Ezh2 on the stress responses. 6. To measure the level of CpG methylation in the promoter region of BDNF in thermal treatments and free-fed, 12-hour fasted, and re-fed chicks during post-natal day 3, which is the critical period for feed-control establishment, and 10 days later to evaluate longterm effects. 7. The phenotypic effect of antisense “knock down” of the transmethylaseDNMT 3a. Background: The growing demand for improvements in poultry production requires an understanding of the mechanisms governing stress responses. Two of the major stressors affecting animal welfare and hence, the poultry industry in both the U.S. and Israel, are feed intake and thermal responses. Recently, it has been shown that the regulation of energy intake and expenditure, including feed intake and thermal regulation, resides in the hypothalamus and develops during a critical post-hatch period. However, little is known about the regulatory steps involved. The hypothesis to be tested in this proposal is that epigenetic changes in the hypothalamus during post-hatch early development determine the stress-response set point for both feed and thermal stressors. The ambitious goals that were set for this proposal were met. It was established that both stressors i.e. feed and thermal stress, can be manipulated during the critical period of development at day 3 to induce resilience to stress later in life. Specifically it was established that unfavorable nutritional conditions during early developmental periods or heat exposure influences subsequent adaptability to those same stressful conditions. Furthermore it was demonstrated that epigenetic marks on the promoter of genes involved in stress memory are altered both during stress, and as a result, later in life. Specifically it was demonstrated that fasting and heat had an effect on methylation and acetylation of histone 3 at various lysine residues in the hypothalamus during exposure to stress on day 3 and during stress challenge on day 10. Furthermore, the enzymes that perform these modifications are altered both during stress conditioning and challenge. Finally, these modifications are both necessary and sufficient, since antisense "knockdown" of these enzymes affects histone modifications, and as a consequence stress resilience. DNA methylation was also demonstrated at the promoters of genes involved in heat stress regulation and long-term resilience. It should be noted that the only goal that we did not meet because of technical reasons was No. 7. In conclusion: The outcome of this research may provide information for the improvement of stress responses in high yield poultry breeds using epigenetic adaptation approaches during critical periods in the course of early development in order to improve animal welfare even under suboptimum environmental conditions.
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Contreras, Claudia Torres, Lina María Vargas Escobar, Jorge Yecid Triana Rodríguez, and Wilson Cañon-Montañez. Spiritual Care Competency in Nursing: An Integrative Literature Review Protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0081.

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Review question / Objective: To review studies with perspectives and intervention strategies for the formation and education in spiritual care for both professionals and nursing students. Condition being studied: Development of empirical studies in the field of nursing education that allow to visualize the developments in the formation of competence in spiritual care, investigating the educational interventions and pedagogical strategies implemented in the formation of nursing professionals and nurses in this specific field. Information sources: Electronic databases: Medline (via PubMed), ProQuest (via EBSCO), Scopus, LILACS and BDENF (via Biblioteca Virtual en Salud – BVS) and SciELO. Scopus, Medline (via PubMed) and LILACS.
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Edgar, Alexander, Lynne Goodwin, Camille Wong, and Dali Yang. Aging and Lifetimes Program FY 2022 Annual Report - Part I: Update to BDNPA-BDNPF phase diagram. Office of Scientific and Technical Information (OSTI), October 2022. http://dx.doi.org/10.2172/1896418.

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7

Campbell, Stephen L. Distributional Convergence of BDF (Backward Differentiation Formulas) Approximations to Solutions of Descriptor Systems. Fort Belvoir, VA: Defense Technical Information Center, November 1987. http://dx.doi.org/10.21236/ada190819.

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8

Al sada, Adnan M. A Literature Review of Empowerment With a Suggested Empowerment Model for the BDF. Fort Belvoir, VA: Defense Technical Information Center, December 2003. http://dx.doi.org/10.21236/ada420235.

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9

Yahav, Shlomo, John Brake, and Noam Meiri. Development of Strategic Pre-Natal Cycling Thermal Treatments to Improve Livability and Productivity of Heavy Broilers. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7593395.bard.

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Abstract:
The necessity to improve broiler thermotolerance and live performance led to the following hypothesis: Appropriate comprehensive incubation treatments that include significant temperature management changes will promote angiogenesis and will improve acquisition of thermotolerance and carcass quality of heavy broilers through epigenetic adaptation. It was based on the following questions: 1. Can TM during embryogenesis of broilers induce a longer-lasting thermoregulatory memory (up to marketing age of 10 wk) that will improve acquisition of thermotolerance as well as increased breast meat yield in heavy broilers? 2. The improved sensible heat loss (SHL) suggests an improved peripheral vasodilation process. Does elevated temperature during incubation affect vasculogenesis and angiogenesis processes in the chick embryo? Will such create subsequent advantages for heavy broilers coping with adverse hot conditions? 3. What are the changes that occur in the PO/AH that induce the changes in the threshold response for heat production/heat loss based on the concept of epigenetic temperature adaptation? The original objectives of this study were as follow: a. to assess the improvement of thermotolerance efficiency and carcass quality of heavy broilers (~4 kg); b. toimproveperipheral vascularization and angiogenesis that improve sensible heat loss (SHL); c. to study the changes in the PO/AH thermoregulatory response for heat production/losscaused by modulating incubation temperature. To reach the goals: a. the effect of TM on performance and thermotolerance of broilers reared to 10 wk of age was studied. b. the effect of preincubation heating with an elevated temperature during the 1ˢᵗ 3 to 5 d of incubation in the presence of modified fresh air flow coupled with changes in turning frequency was elucidated; c.the effect of elevated temperature on vasculogenesis and angiogenesis was determined using in ovo and whole embryo chick culture as well as HIF-1α VEGF-α2 VEGF-R, FGF-2, and Gelatinase A (MMP2) gene expression. The effects on peripheral blood system of post-hatch chicks was determined with an infrared thermal imaging technique; c. the expression of BDNF was determined during the development of the thermal control set-point in the preoptic anterior hypothalamus (PO/AH). Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” Recently, Piestunet al. (2008) demonstrated for the first time that TM (an elevated incubation temperature of 39.5°C for 12 h/d from E7 to E16) during the development/maturation of the hypothalamic-hypophyseal-thyroid axis (thermoregulation) and the hypothalamic-hypophyseal-adrenal axis (stress) significantly improved the thermotolerance and performance of broilers at 35 d of age. These phenomena raised two questions that were addressed in this project: 1. was it possible to detect changes leading to the determination of the “set point”; 2. Did TM have a similar long lasting effect (up to 70 d of age)? 3. Did other TM combinations (pre-heating and heating during the 1ˢᵗ 3 to 5 d of incubation) coupled with changes in turning frequency have any performance effect? The improved thermotolerance resulted mainly from an efficient capacity to reduce heat production and the level of stress that coincided with an increase in SHL (Piestunet al., 2008; 2009). The increase in SHL (Piestunet al., 2009) suggested an additional positive effect of TM on vasculogenesis and angiogensis. 4. In order to sustain or even improve broiler performance, TM during the period of the chorioallantoic membrane development was thought to increase vasculogenesis and angiogenesis providing better vasodilatation and by that SHL post-hatch.
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10

Tsai, W. H., N. G. Cave, and F. J. Boerio. Characterization of Interphases between PMDA/4-BDAF Polyimides and Silver and Graphite Substrates Using X-Ray Photoelectron Spectroscopy. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada235567.

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