scholarly journals Neurotrophic factors concentration in rat brain at the experimental coma

2013 ◽  
Vol 94 (5) ◽  
pp. 695-699 ◽  
Author(s):  
V A Kashuro ◽  
E G Batotsyrenova ◽  
N L Elaeva ◽  
U N Savenko ◽  
N V Lapina ◽  
...  
Keyword(s):  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Protein S ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Acidic Protein ◽  
Ethanol Administration ◽  
S 100 ◽  
Protein Serum ◽  
Glial Fibrillar Acidic Protein

Aim. To study the changes of neurotrophic factors concentrations depending on stage of intoxication with deprivation substances (ethanol or sodium oxybutirate) in rats. Methods. Experiments were performed on male white laboratory rats. Control and experimental groups included 10 animals each. Half-lethal doses of a deprivation substance (ethanol or sodium oxybutirate) were introduced intraperitoneally 3, 6, 12, 24 and 72 hours before blood specimen collection. Neuron-specific enolase, S-100 protein, brain-derived neurotrophic factor, pigment epithelium-derived factor, glial fibrillary acidic protein serum levels were measured by enzyme immunoassay. Results. At single infusion of mean lethal dose of sodium oxybutyrate S-100 protein serum level significantly increased after 6 hours compared to control and stayed elevated during the first 24 hours. The levels of neurotrophic and neuroprotective factors also significantly increased 3 and 6 hours after the drug administration. The toxic dose of ethanol have significantly increased (over than 1.8 times compared to the controls) the concentration of protein S-100 in rats after 3 hours. The maximum increase in the protein S-100 level (by 2.6 times and over) was noted 12 hours after the toxicant administration. Glial fibrillar acidic protein concentration was 2.9 times higher compared to controls 3 hours after and 1.9 times higher 6 hours after higher the ethanol administration (р 0.05). The concentration of brain - derived neurotrophic factor has also increased from 3 to 12 hours after the toxicant administration, and was 2.1 to 2.4 times higher compared to intact animals. Conclusion. Studying of neurotrophic factors brain in plasma showed that the development of hypoxia, accompanying coma, leads to higher serum levels of S-100 protein, brain-derived neurotrophic factor and glial fibrillar acidic protein. The increase in the concentration of S-100 is a marker for the presence of brain damage. The observed increase of glial fibrillar acidic protein in experiments with ethanol may indicate its more severe brain tissue damage compared to sodium oxybutyrate.

Brain-derived neurotrophic factor is associated with coronary macrophage infiltrates in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
M Camilli ◽  
M Russo ◽  
M Del Buono ◽  
F Gurguglione ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
C Reactive Protein ◽  
St Segment Elevation ◽  
Protein Levels ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
St Segment

Abstract Background Brain-derived neurotrophic factor (BDNF) is a neurotrophine that plays a key role in the regulation of both central and peripheral nervous system. Moreover, BDNF is secreted in multiple tissues and exerts systemic, autocrine, and paracrine effects in the cardiovascular system. Of importance, BDNF expression was enhanced in macrophages and smooth muscle cells in atherosclerotic coronary arteries and may be involved in thrombus formation. Thus, BDNF has been suggested as an important link between inflammation and thrombosis, potentially involved in the pathogenesis of acute coronary syndrome (ACS). Purpose In our study we aimed at assessing serum levels of BDNF in patients with ACS, evaluating differences according to clinical presentation [ST-segment elevation myocardial infarction (STEMI) vs. Non-ST-segment elevation ACS (NSTE-ACS)]. Moreover, we assessed the presence of optical coherence (OCT)-defined macrophage infiltrates (MØI) in the culprit vessel of ACS patients and evaluated their relationship with BDNF levels. Methods ACS patients were prospectively selected. Blood samples were collected at admission and serum levels of BDNF were subsequently assessed. Presence of OCT-defined MØI along the culprit vessel was assessed. Results 166 ACS patients were enrolled [mean age 65.3±11.9 years, 125 (75.3%) male, 109 STEMI, 57 NSTE-ACS]. Serum levels of BDNF were higher among STEMI patients compared with NSTE-ACS [median (IQR) 2.48 pg/mL (1.54–3.34) vs. 2.12 pg/mL (1.34–2.47), p=0.007], while C-reactive protein levels did not differ between the two groups. OCT assessment was performed in 53 patients and MØI were detected in 27 patients. Of importance, patients with MØI in the culprit vessel had higher levels of BDNF compared with patients without MØI [median (IQR) 2.23 pg/mL (1.38–2.53) vs. 1.41 pg/mL (0.93–2.07), p=0.023], while C-reactive protein levels did not differ between the two groups. Of note, at multivariate regression analysis BDNF levels were independent predictor of MØI [OR: 2.20; 95% CI (1.02–4.74), p=0.043]. Conclusions Serum levels of BDNF may reliable identify the presence of local macrophage inflammatory infiltrates in patients with ACS. Moreover, BDNF levels are higher in patients with STEMI compared with NSTE-ACS. Taken together, these data suggest that BDNF may represent an interesting link between local inflammatory activation and enhanced thrombosis in ACS. BDNF serum levels Funding Acknowledgement Type of funding source: None

scholarly journals Watching Neurons Hand Off Molecules

2002 ◽  
Vol 10 (1) ◽  
pp. 3-34
Author(s):  
Stephen W. Carmichael
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Target Cells ◽  
Nerve Growth ◽  
Hand Off ◽  
Presynaptic Neurons

Since the discovery of nerve growth factor, it has been thought that neurotrophic factors are released or secreted from target cells. However, more recently it has been suggested that a specific neurotrophic factor known as brain-derived neurotrophic factor (BDNF) may reach target cells directly from pre-synaptic axons. It has not been known how these molecules get from the neuron in which they are produced to the target cells. Keigo Kohara, Akihiko Kitamura, Mieko Morishima, and Tadaharu Tsumoto have demonstrated that BDNF is transported anterogradely from presynaptic neurons to target neurons.

Brain-derived neurotrophic factor serum levels in heroin-dependent patients after 26weeks of withdrawal

2016 ◽  
Vol 65 ◽  
pp. 150-155 ◽  
Author(s):  
Kai Zhang ◽  
Haifeng Jiang ◽  
Qiaoyang Zhang ◽  
Jiang Du ◽  
Yuan Wang ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor

A close correlation between plasma and serum levels of brain-derived neurotrophic factor (BDNF) in healthy volunteers

2010 ◽  
Vol 14 (3) ◽  
pp. 220-222 ◽  
Author(s):  
Reiji Yoshimura ◽  
Atsuko Sugita-Ikenouchi ◽  
Hikaru Hori ◽  
Wakako Umene-Nakano ◽  
Kenji Hayashi ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Neurotrophic Factor ◽  
Close Correlation ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor

Poster #113 BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF), NEUROTROPHIN 3 (NTF3), NEUROTROPHIN 4 (NTF4) AND GLIAL-DERIVED NEUROTROPHIC FACTOR (GDNF) SERUM LEVELS IN SCHIZOPHRENIA

2012 ◽  
Vol 136 ◽  
pp. S132-S133
Author(s):  
Anna Leszczynska-Rodziewicz ◽  
Maria Skibinska ◽  
Pawel Kapelski ◽  
Aleksandra Rajewska-Rager ◽  
Joanna Pawlak ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Neurotrophin 3 ◽  
Glial Derived Neurotrophic Factor

scholarly journals OP0086 GENDER INFLUENCE ON CLINICAL MANIFESTATIONS, DEPRESSIVE SYMPTOMS AND BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF) SERUM LEVELS IN PATIENTS AFFECTED BY FIBROMYALGIA

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 47.2-47
Author(s):  
C. Gioia ◽  
B. Lucchino ◽  
C. Iannuccelli ◽  
G. Dolcini ◽  
M. DI Franco
Keyword(s):  
Depressive Symptoms ◽  
Serum Level ◽  
Mood Disorders ◽  
Neurotrophic Factor ◽  
Fibromyalgia Impact Questionnaire ◽  
Clinical Manifestations ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Control Group ◽  
Males And Females

Background:Fibromyalgia (FM) is a common rheumatic disease characterized by chronic widespread pain, sleep and mood disorders. A higher prevalence of FM in women compared with men is well known, although the specific differences in clinical manifestations related to gender are still poorly defined. Brain-Derived Neurotrophic Factor (BDNF) is an endogenous growth factor that gained attention for its potential as biomarker of several diseases, including FM and depression.Objectives:The aims of this study were to investigate gender-related difference among males and females affected by FM in clinical manifestations, depressive features and BDNF serum level, evaluating also the diagnostic potential of the latter.Methods:We consecutively enrolled adult patients affected by FM (ACR 2016) referring to our out-patient clinic. Each subject underwent clinical and answered to questionnaires for the severity of FM symptoms (Revised Fibromyalgia Impact Questionnaire, R-FIQ) and depressive symptoms (Beck Depression Inventory-II, BDI-II). We collected blood samples from a subgroup of patients of both sexes, matched for age, for BDNF serum level dosage through ELISA. BDNF levels were assessed also in a control group, matched for sex and age.Results:The cohort was composed by 201 FM patients (172 F, 29 M), mean age 49.13. Females showed higher values of R-FIQ total score (p=0,0005) as well the specific items of the R-FIQ for pain (p=0,013), fatigue (p=0,014), memory problems (p=0,007), tenderness to touch (p<0,0001), balance problems (p<0,0001) and sensitivity to environmental stimuli (p=0,012) when compared with males (fig. 1). There was no difference in BDI-II between males and females, but notably male patients reported a significantly higher frequency of coexisting depressive disorder (p=0,038) (fig. 2). Serum BDNF levels were evaluated in 40 FM patients and 40 healthy controls (HC) (F:M 1:1). BDNF levels were significantly lower in FM patients compared with HC (p<0,0001). Among FM patients, BDNF levels were lower in males compared with females (p<0,0001) (fig.3). BDNF did not correlate with any clinical and clinimetric parameter. BDNF showed a good diagnostic performance (AUC=0,89, CI95%=0,82-0,9630, p<0,0001) (fig. 4). At a cut-off value <6,47 ng/dl, BDNF showed a specificity of 75% and a sensibility of 92,31%,(CI 95%=79,68-97.35) for FM identification (LR=3,692).Conclusion:FM clinical manifestations are strongly dependant from gender. While females present a more severe disease and a higher burden of symptoms, mood disorders tend to be a major characteristic of males with FM. Reduced BDNF serum levels have been reported as typical of depressive disorders. Our findings of lower BDNF levels in male FM patients compared to females support this hypothesis. BDNF have potential as biomarker of the disease and should be validated in larger cohorts.References:[1]Sarzi-Puttini et al. Nature Reviews 2020[2]Colucci-D’Amato et al. Int J Molecular Sciences 2020[3]Nugraha et al. Rheumatol Int 2012[4]Schmitt et al. Ann Med 2016[5]Melchior et al. Neuroscience 2016[6]Stefani et al. Neuroscience Letters 2012Disclosure of Interests:None declared

scholarly journals Interferon beta-1a induces expression of brain-derived neurotrophic factor in human T lymphocytes in vitro and not in vivo

2020 ◽  
Vol 15 (1) ◽  
pp. FNL38 ◽  
Author(s):  
Zarlascht Karmand ◽  
Hans-Peter Hartung ◽  
Oliver Neuhaus
Keyword(s):  
T Cell ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Peripheral Blood Lymphocytes ◽  
T Cell Proliferation ◽  
Bdnf Expression ◽  
Healthy Donors

Aim: To detect IFN β-1a-induced expression of brain-derived neurotrophic factor (BDNF) to undermine the hypothesis of IFN β-1a-associated neuroprotection in multiple sclerosis (MS). Methods: The influence of IFN β-1a on in vitro activated peripheral blood lymphocytes from healthy donors was tested. Proliferation analyses were made to detect T-cell growth. BDNF expression was measured by standard ELISA. To assess the influence of IFN β-1a on BDNF expression in vivo, BDNF serum levels of MS patients treated with IFN β-1a were compared with those of untreated patients. Results: IFN β-1a inhibited T-cell proliferation dose dependently. It induced BDNF expression at middle concentrations. MS patients treated with IFN β-1a exhibited significantly lower BDNF serum levels than untreated patients. Conclusion: IFN β-1a may promote neuroprotection by inducing BDNF expression, but its importance in vivo remains open.

scholarly journals Serum Tryptophan, Tryptophan Catabolites and Brain-derived Neurotrophic Factor in Subgroups of Youngsters with Autism Spectrum Disorders

2018 ◽  
Vol 17 (8) ◽  
pp. 626-639 ◽  
Author(s):  
Heidi Ormstad ◽  
Vesna Bryn ◽  
Robert Verkerk ◽  
Ola H. Skjeldal ◽  
Bente Halvorsen ◽  
...  
Keyword(s):  
Autism Spectrum Disorders ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Autism Spectrum ◽  
Childhood Autism ◽  
Total Blood ◽  
Healthy Control ◽  
Tryptophan Catabolites ◽  
Spectrum Disorders

Background: There is evidence that changes in neuro-immune responses coupled with dysfunctions in serotonin metabolism underpin the pathophysiology of autism spectrum disorders (ASD). Objective: This study aimed to delineate whether ASD subgroups or characteristics show aberrations in tryptophan and brain-derived neurotrophic factor (BDNF) metabolism. Methods: 65 individuals with ASD (diagnosed according to ICD criteria) and 30 healthy control patients were included. Measured were serum levels of tryptophan, kynurenine (KYN), kynurenic acid (KA), quinolinic acid (QA), BDNF and PRO-BDNF and total blood 5-HT and 5-OH-tryptophan (5-HTP). Results: Elevated BDNF levels and lower tryptophan and KA levels were characteristics of both childhood autism and intellectual disability disorder, whilst elevated tryptophan and lower 5-HT synthesis were hallmarks of Asperger syndrome. A pathological MRI was associated with elevated tryptophan and lowered KA. Abnormal EEG results and dysmorphology were both associated with an elevated BDNF/ PRO-BDNF ratio. Any brain pathology and gastro-intestinal symptoms were accompanied by lowered KA. Conclusions: Increased BDNF production and changes in the metabolism of tryptophan are associated with many ASD characteristics, showing particularly strong associations with childhood autism and Intellectual and Developmental Disabilities. Peripheral BDNF and tryptophan metabolism appear to take part in the pathophysiology of autism spectrum disorders and their phenotypes.

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