No effect of escitalopram versus placebo on brain-derived neurotrophic factor in healthy individuals: a randomised trial

2015 ◽  
Vol 28 (2) ◽  
pp. 101-109 ◽  
Author(s):  
Ulla Knorr ◽  
Pernille Koefoed ◽  
Mia H. Greisen Soendergaard ◽  
Maj Vinberg ◽  
Ulrik Gether ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Whole Blood ◽  
Neurotrophic Factor ◽  
Messenger Rna ◽  
Randomised Trial ◽  
Significant Negative Correlation ◽  
Brain Derived Neurotrophic Factor ◽  
Healthy Individuals ◽  
Bdnf Mrna ◽  
Significant Difference

ObjectiveBrain-derived neurotrophic factor (BDNF) seems to play an important role in the course of depression including the response to antidepressants in patients with depression. We aimed to study the effect of an antidepressant intervention on peripheral BDNF in healthy individuals with a family history of depression.MethodsWe measured changes in BDNF messenger RNA (mRNA) expression and whole-blood BDNF levels in 80 healthy first-degree relatives of patients with depression randomly allocated to receive daily tablets of escitalopram 10 mg versus placebo for 4 weeks.ResultsWe found no statistically significant difference between the escitalopram and the placebo group in the change in BDNF mRNA expression and whole-blood BDNF levels. Post hoc analyses showed a statistically significant negative correlation between plasma escitalopram concentration and change in whole-blood BDNF levels in the escitalopram-treated group.ConclusionThe results of this randomised trial suggest that escitalopram 10 mg has no effect on peripheral BDNF levels in healthy individuals.

Photochemical stroke and brain-derived neurotrophic factor (BDNF) mRNA expression

Neuroreport ◽  
1992 ◽  
Vol 3 (6) ◽  
pp. 473-476 ◽  
Author(s):  
Maria Cristina Comelli ◽  
Maria Serena Seren ◽  
Diego Guidolin ◽  
Radmila M. Manev ◽  
Marco Favaron ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Mrna

scholarly journals Brain-derived neurotrophic factor, epigenetics in stroke skeletal muscle, and exercise training

2019 ◽  
Vol 5 (3) ◽  
pp. e331 ◽  
Author(s):  
Alice S. Ryan ◽  
Huichun Xu ◽  
Frederick M. Ivey ◽  
Richard F. Macko ◽  
Charlene E. Hafer-Macko
Keyword(s):  
Skeletal Muscle ◽  
Dna Methylation ◽  
Exercise Training ◽  
Mrna Expression ◽  
Neurotrophic Factor ◽  
Methylation Status ◽  
Brain Derived Neurotrophic Factor ◽  
Vastus Lateralis Muscle ◽  
Bdnf Mrna ◽  
Blood Draw

Objective(1) To compare paretic (P) vs nonparetic (NP) skeletal muscle brain-derived neurotrophic factor (BDNF) and the effects of resistive training (RT) on systemic and skeletal muscle BDNF mRNA expression in stroke; and (2) to compare the DNA methylation profile for BDNF and BDNFAS (BDNF antisense RNA) between P and NP muscle and the effects of aerobic exercise training (AEX) on DNA methylation in stroke.MethodsIn this longitudinal investigation, participants (50–76 years) with chronic stroke underwent a fasting blood draw, a 12-week (3×/week) RT intervention (n = 16), and repeated bilateral vastus lateralis muscle tissue biopsies (n = 10) with BDNF expression determined by RT-PCR. Five stroke survivors completed 6 months of AEX (3×/week) and had bilateral muscle biopsies. DNA methylation status in gene BDNF and BDNFAS was assessed by Illumina 450k methylation array.ResultsP muscle had ∼45% lower BDNF mRNA expression than NP muscle (6.79 ± 1.30 vs 10.52 ± 2.06 arbitrary units [AU], p < 0.05), and P muscle exhibited differential methylation status in the DNA sequences of BDNF (3 CpG [5′-C-phosphate-G-3′] sites, p = 0.016–0.044) and BDNFAS (1 CpG site, p = 0.016) compared to NP. Plasma BDNF and muscle BDNF messenger RNA (mRNA) expression did not significantly change after RT. BDNFAS DNA methylation increased after AEX in P relative to NP muscle (p = 0.017).ConclusionsThis is the first evidence that stroke hemiparesis reduces BDNF skeletal muscle expression, with our findings identifying methylation alterations on the DNA sequence of BDNF and BDNFAS gene. Preliminary results further indicate that AEX increases methylation in BDNFAS gene, which presumably could regulate the expression of BDNF.

scholarly journals Brain-derived neurotrophic factor and TrkB levels in mice that lack vesicular zinc: Effects of age and sex

2018 ◽  
Author(s):  
Brendan B. McAllister ◽  
Nicoline Bihelek ◽  
Richelle M. Mychasiuk ◽  
Richard H. Dyck
Keyword(s):  
Mrna Expression ◽  
Knockout Mice ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Receptor Kinase ◽  
Wild Type ◽  
Bdnf Mrna ◽  
Protein Levels ◽  
Intact Brain

ABSTRACTIn certain neurons, zinc ions are stored in synaptic vesicles by zinc transporter 3 (ZnT3). Vesicular zinc can then be released synaptically to modulate myriad targets. In vitro evidence indicates that these targets may include brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB). But the effects of vesicular zinc on BDNF and TrkB in the intact brain are unclear. Studies of mice that lack ZnT3 – and, as a result, vesicular zinc – have shown abnormalities in BDNF and TrkB levels, but results have been mixed and are therefore difficult to interpret. This might be caused by differences in the age or sex of mice tested. In the present study, we measured BDNF and TrkB levels in the hippocampus and neocortex, comparing wild type and ZnT3 knockout mice of both sexes at two ages (5 and 12 weeks). We also examined BDNF mRNA expression and protein levels at an intermediate age (8-10 weeks). We found that, regardless of age or sex, BDNF and TrkB protein levels did not differ between wild type and ZnT3 knockout mice. There were sex-specific differences in BDNF protein and mRNA expression, however. BDNF protein levels increased with age in female mice but not in males. And in females, but not males, ZnT3 KO mice exhibited great hippocampal BDNF mRNA expression than wild type mice. We conclude that, at least in naïve mice housed under standard laboratory conditions, elimination of vesicular zinc does not affect BDNF or TrkB protein levels.

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