The current study looked at a population of patients with major depressive disorder (N = 107) to examine the association between the BDNFVal66Met polymorphism, resting state EEG alpha power, and depression severity.
Associations between the BDNFval66met polymorphism and both depression status and treatment response were investigated using logistic regression models.
To evaluate the effect of vortioxetine combined with cognitive behaviour intervention on the level of brain-derived neurotrophic factor (BDNF) in the serum of patients with depression and its therapeutic effect.
Furthermore, acne vulgaris patients with depression showed lower serum BDNF levels (10.96 ± 2.12 ng/ml) compared with acne vulgaris patients without depression (13.85 ± 2.47 ng/ml), as well as with healthy control (14.35 ± 2.70 ng/mg; both P < 0.05).
Therefore, in this review burnout and depression are discussed on the basis of biological parameters, mainly heart rate variability (HRV) and brain-derived neurotrophic factor (BDNF), which are crucial to the stress response system.
These results strongly implicate changes in BDNF levels in serum and the nucleus accumbens in the pathophysiology and treatment of early life combined stress-induced depression and highlight the therapeutic potential of escitalopram and new generation antipsychotic blonanserin for treatment-resistant refractory depression.
Brain-derived neurotrophic factor (BDNF) has appeared to play a critical role in certain neurobiological modifications that may otherwise lead to schizophrenia or depression.
We found evidence that supported the hypothesis that BDNFVal66Met polymorphism moderated the relationship between stress and depression, despite the fact that many included individual studies did not show this effect.
However, BDNFrs7103411 and rs6265 similarly predicted worse treatment response over 6 wk in clinical subtypes of depression such as melancholic depression only (rs7103411: TT < CC, p = 0.003; rs6265: GG < AA, p = 0.001).
We investigated the effect of a daily low dose of a phosphodiesterase (PDE) type 5 inhibitor (tadalafil, 5 mg) on depression and levels of brain-derived neurotrophic factor (BDNF) in patients with ED.
According to this rationale, we investigated the role of two functional polymorphisms in the genes coding for the serotonin transporter (5-HTTLPR) and the brain-derived neurotrophic factor (BDNF Val66Met), and rTMS response in a group of 36 drug resistant patients affected by mood disorders. rTMS treatment significantly improved depression symptomatology (p<0.0001) and the response was significantly greater in 5-HTTLPR LL homozygotes compared to S allele carriers (p=0.007) and in BDNF Val/Val homozygotes compared to Met allele carriers (p=0.024).
This study was to examine the chronic stress × BDNFVal66Met interaction in job-related depression in the healthcare workers in a Chinese Han population, which has not been reported yet.
Neither 5-HTTLPR or BDNF genotypes separately, nor in interaction with each other had any relation to depression, however in an environment adjusted model a two-way interaction and a three-way interaction effect was found.
Our findings show an association between low serum BDNF and SI in individuals with less than severe and non-active suicidal intent, suggesting that the individual symptom of suicidality may extend the neurotrophic hypothesis of depression to include suicidal ideation within MDD.