Probabilistic tractography revealed higher FA in the uncinate fasciculus (UF) for BDNF val/val genotype relative to met-carriers, particularly in individuals with high depression severity.
However, one specific set of genes, the brain derived neurotrophic factor (BDNF), specifically the Val66Met polymorphism, may play a crucial role in AD-related depression.
In 305 healthy subjects, BDNFVal66Met genotypes were compared in terms of trait depression, neural function (EEG during a resting state) and cognitive performance.
However, presumed elevated BDNF levels among individuals with the Val/Val genotype, might confer increased responsivity to contextual challenges, thus fostering vulnerability to depression.
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.
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).
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.
The BDNF gene is characterized by a functional polymorphism, which has been associated with stress-related disorders such as anxiety-related syndromes and depression, prompting us to examine individual responses by Genotype and Sex to a standardized social stress paradigm.
Suicidal ideation was independently associated with depression and physical disability at 1 week and with living alone, anxiety, advanced cancer stage, and the BDNF met allele (but not with genetic polymorphisms on serotonergic system) at 1 year after breast surgery.
Clinical and preclinical studies have demonstrated that depression, one of the most common psychiatric illnesses, is associated with reduced levels of neurotrophic factors, including brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), contributing to neuronal atrophy in the prefrontal cortex (PFC) and hippocampus, and reduced hippocampal adult neurogenesis.
The BDNF Met/Met genotype was independently associated with prevalent (odds ratio = 2.63, 95% confidence interval = 1.12-6.14) and persistent (odds ratio = 8.07, 95% confidence interval = 1.26-51.6) depression.
This work establishes BDNF<sup>Val66Met</sup> genotype as a regulator of behavioral despair, and identifies new biological targets of BDNF genetic variation relevant to stress-inducible disorders such as depression.
Discussion The dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNFVal66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels.