Call us toll-free

KW - brain-derived neurotrophic factor

T1 - Brain-derived neurotrophic factor gene polymorphisms and mirtazapine responses in Koreans with major depression

Approximate price

Pages:

275 Words

$19,50

for the neurotrophic hypothesis of depression.

Around the same time it was noticed that tuberculosis patients, prescribed a different drug, isometimes experienced a of pre-existing depression. Isoniazid inhibits (slows down or prevents the activity of) the substance monoamine oxidase (MAO). MAO is important because it breaks down monoamine neurotransmitters. As MAO destroys monoamines, inhibiting MAO would have the net effect of the levels of monoamines available for neuron to neuron communication.

Such monoamine oxidase inhibitors (or MAOIs) became the first generation of antidepressants.

Brain-derived neurotrophic factor (BDNF) is a candidate molecule for influencing the clinical response to antidepressant treatment. The aims of this study were to determine the relationship between the Val66Met polymorphism in the BDNF gene and the response to mirtazapine in 243 Korean subjects with major depressive disorder (MDD). The reduction in the Hamilton Depression score over the 8-week treatment period was not influenced by BDNF V66M genotypes. A marginal effect of genotype on somatic anxiety score was observed at baseline (P = 0.047 in the dominant model). However, genotype-time interaction had no effect on somatic anxiety score after the 8-week a treatment period. Plasma BDNF levels tended to increase during mirtazapine treatment, although without statistical significance (P = 0.055). After 8 weeks of mirtazapine treatment, plasma BDNF levels were higher in Met allele homozygotes (1499.7 ± 370.6 ng/mL) than in Val allele carriers (649.7 ± 158.5 ng/mL, P = 0.049). Our results do not support the hypothesis that the Val66Met promoter polymorphism in the BDNF gene influences the therapeutic response to mirtazapine in Korean MDD patients. However, our data indicate that this polymorphism results in increased plasma BDNF after mirtazapine treatment.

Brain-derived neurotrophic factor - Wikipedia

Depression is currently among the four major diseases affecting the world population and is linked to high rates of impairment and mortality [-], and can be defined as a disorder with heterogeneous biological bases with a chance of affecting 10% -30% of women and 7% -15% of men throughout their lives. Clinical and preclinical studies suggest that Brain-Derived Neurotrofic Factor (BNDF) expression could be involved in behavioral phenomena linked to depression, and that modulation of this neurotrophin would also mediate the action of antidepressants [].

(4) Genetically altered mice with disrupted BDNF functions lack spontaneous depressive phenotypes and evidences from single-nucleotide polymorphism are controversial [6] . The diverse regionally-specific roles of BDNF in brain permit itself to be a modulating factor on activity-dependent plasticity within emotional processing networks, the integrity of which will be compromised under mood disorders [7] .Collectively, BDNF might lie in the genesis of bipolar disorders and reflect the sensitivity under risky environments, stressful conditions for instance. However, current studies on neurotrophin modulating-antidepressants are still prospective, and may finally bring us a full picture of BNDF roles in mood disorders.

Brain-derived neurotrophic factor, also known as BDNF, is a ..

The Brain-Derived Neurotrofic Factor (BDNF) is one of the most important neurotrophins in the brain and it is suggested influences the activity of the serotonergic, noradrenergic and dopaminergic pathways. In the last few years, it has been hypothesized that BDNF level is related with depression and sleep. Several studies show that depressive subjects present low levels of BDNF in the brain. Poor sleep quality is also related with alterations in the BDNF concentration. Some authors argue that most of the cases show that impaired sleep quality increases the stress and, consequently, the vulnerability to depressive disorders, suggesting that there is a relationship between sleep, depression and BDNF levels.

N2 - Brain-derived neurotrophic factor (BDNF) is a candidate molecule for influencing the clinical response to antidepressant treatment. The aims of this study were to determine the relationship between the Val66Met polymorphism in the BDNF gene and the response to mirtazapine in 243 Korean subjects with major depressive disorder (MDD). The reduction in the Hamilton Depression score over the 8-week treatment period was not influenced by BDNF V66M genotypes. A marginal effect of genotype on somatic anxiety score was observed at baseline (P = 0.047 in the dominant model). However, genotype-time interaction had no effect on somatic anxiety score after the 8-week a treatment period. Plasma BDNF levels tended to increase during mirtazapine treatment, although without statistical significance (P = 0.055). After 8 weeks of mirtazapine treatment, plasma BDNF levels were higher in Met allele homozygotes (1499.7 ± 370.6 ng/mL) than in Val allele carriers (649.7 ± 158.5 ng/mL, P = 0.049). Our results do not support the hypothesis that the Val66Met promoter polymorphism in the BDNF gene influences the therapeutic response to mirtazapine in Korean MDD patients. However, our data indicate that this polymorphism results in increased plasma BDNF after mirtazapine treatment.

Order now
  • [The neurotrophic hypothesis of depression] (2016) | …

    [The neurotrophic hypothesis of depression] ..

  • derived neurotrophic factor (bdnf) ..

    A neurotrophic hypothesis of depression and ..

  • Role of neurotrophic factors in depression - ScienceDirect

    Role of neurotrophic factors in depression

Order now

Brain-derived neurotrophic factor: role in depression …

Dietary Patterns and Nutrient Deficits
In addition to exploring markers of oxidative stress, RDs also should evaluate clients' dietary patterns and possible nutrient deficiencies, as the brain is an organ dependent on a constant supply of nutrients. There's clear evidence that dietary patterns and specific nutrients are vital to the mitigation of inflammation, oxidative stress/mitochondrial dysfunction, and gut dysbiosis.3 Nutrients also are necessary to support methylation, neurobiological networks, and hormone signaling pathways that modulate mood, appetite, sleep, neurogenesis, and cognitive function.16 Several metabolic actors including insulin, GABA (gamma-Aminobutyric acid), brain-derived neurotrophic factor (BDNF), and other gut hormones play roles in stress-related and affective disorders.17

setting the foundation for the neurotrophic hypothesis of depression

AB - Background: Major depressive disorder is a leading debilitating disease known to occur at a two-fold higher rate in women than in men. The neurotrophic hypothesis of depression suggests that loss of brain-derived neurotrophic factor (BDNF) may increase susceptibility for depression-like behavior, although direct evidence is lacking. Methods: Using the chronic unpredictable stress (CUS) paradigm, we investigated whether male and female mice with inducible BDNF deletion in the forebrain were more susceptible to depression-related behavior. Results: We demonstrate that in certain behavioral measures the loss of BDNF lowers the threshold for female mice studied at random throughout estrus to display anxiogenic and anhedonic behaviors after chronic stress compared with wild-type female mice. However, the loss of BDNF in forebrain does not increase the susceptibility to depression-like behavior in male mice. Conclusions: These gender differences suggest a role for BDNF in mediating some aspects of depression-related behavior in females.

A neurotrophic hypothesis of depression: role ..

AB - Brain-derived neurotrophic factor (BDNF) is a candidate molecule for influencing the clinical response to antidepressant treatment. The aims of this study were to determine the relationship between the Val66Met polymorphism in the BDNF gene and the response to mirtazapine in 243 Korean subjects with major depressive disorder (MDD). The reduction in the Hamilton Depression score over the 8-week treatment period was not influenced by BDNF V66M genotypes. A marginal effect of genotype on somatic anxiety score was observed at baseline (P = 0.047 in the dominant model). However, genotype-time interaction had no effect on somatic anxiety score after the 8-week a treatment period. Plasma BDNF levels tended to increase during mirtazapine treatment, although without statistical significance (P = 0.055). After 8 weeks of mirtazapine treatment, plasma BDNF levels were higher in Met allele homozygotes (1499.7 ± 370.6 ng/mL) than in Val allele carriers (649.7 ± 158.5 ng/mL, P = 0.049). Our results do not support the hypothesis that the Val66Met promoter polymorphism in the BDNF gene influences the therapeutic response to mirtazapine in Korean MDD patients. However, our data indicate that this polymorphism results in increased plasma BDNF after mirtazapine treatment.

Order now
  • Kim

    "I have always been impressed by the quick turnaround and your thoroughness. Easily the most professional essay writing service on the web."

  • Paul

    "Your assistance and the first class service is much appreciated. My essay reads so well and without your help I'm sure I would have been marked down again on grammar and syntax."

  • Ellen

    "Thanks again for your excellent work with my assignments. No doubts you're true experts at what you do and very approachable."

  • Joyce

    "Very professional, cheap and friendly service. Thanks for writing two important essays for me, I wouldn't have written it myself because of the tight deadline."

  • Albert

    "Thanks for your cautious eye, attention to detail and overall superb service. Thanks to you, now I am confident that I can submit my term paper on time."

  • Mary

    "Thank you for the GREAT work you have done. Just wanted to tell that I'm very happy with my essay and will get back with more assignments soon."

Ready to tackle your homework?

Place an order