In our sample, baseline serum BDNF levels did not predictmajor depression and the clinical characteristics of the patients did not predict their BDNF levels.
The gene encoding brain-derived neurotrophic factor (BDNF) has been suggested as a candidate for major depression, and for depression susceptibility in different neurological and psychiatric diseases.
These results suggest that the interactions of BDNF (rs6265) with NTRK2 (rs1387923, rs2769605 and rs1565445) gene polymorphisms likely play an essential role in the development of TRD in Han Chinese MDD patients.
Several studies have linked 5-HT1A C1019G and BDNFG196A (Val66Met) gene polymorphisms to major depressive disorder (MDD) and the actions of antidepressants.
Genotyping for BDNF and GDNF polymorphisms was performed in 298 patients with MDD who started 20 mg paroxetine per day and had their plasma concentrations measured after 6 weeks.
We investigated whether single nucleotide polymorphisms (SNPs) associated with neuroplasticity and activity of monoamine neurotransmitters, such as the brain-derived neurotrophic factor (BDNF, rs6265), the serotonin transporter (SLC6A4, rs25531), the tryptophan hydroxylase 1 (TPH1, rs1800532), the 5-hydroxytryptamine receptor 2A (HTR2A, rs6311, rs6313, rs7997012), and the catechol-O-methyltransferase (COMT, rs4680) genes, are associated with efficacy of transcranial direct current stimulation (tDCS) in major depression.
We found no significant association of either the BDNFG196A or MTHFR C677T polymorphisms with major depressive disorder neither in female nor male group of patients.
Moreover, there was no significant difference in normalized HCV between 5HTTLPR diallelic and triallelic classifications or between the BDNFVal66Met genotypes in MDD patients, although there was a relationship between BDNF Val66Met and ICV.
We examined the effects of BDNF single nucleotide polymorphisms (SNPs) in response to the antidepressants paroxetine and mirtazapine in a sample of 246 geriatric patients with major depression, treated in a double-blind, randomized, 8-week clinical trial.
Recent meta-analyses point towards a pathogenic role of the Val66Met variant of the brain-derived neurotrophic factor (BDNF) in major depressive disorder, specifically in males.
While BDNF was not associated with major depression as a categorical diagnosis, the BDNFrs7124442 TT genotype was significantly related to worse treatment outcome over 6 wk in major depression (p = 0.01) particularly in anxious depression (p = 0.003) in the German sample.
To examine the effect of the BDNFVal66Met polymorphism on hippocampal and amygdala volumes in patients with major depression and in healthy control subjects.
Our study suggests that low BDNF levels may play a pivotal role in the pathophysiology of MDD and that antidepressants may increase BDNF in depressed patients.
Such an association would be consistent with low brain-derived neurotrophic factor mediating the effect of early life adversity on adulthood suicide and major depressive disorder.
Total hippocampal volumes did not significantly vary in MDD participants or controls carrying either the BDNFVal66Met 'Met' (386 participants with MDD and 376 controls) or the 5-HTTLPR short 'S' (310 participants with MDD and 230 controls) risk alleles compared to non-carriers.
1) The age-related decrease in BDNF transcripts observed in control subjects corresponds with further age-related decreases in BDNF and BDNF-dependent gene expression in MDD subjects; 2) most MDD-related genes are frequently age-regulated in both MDD and control subjects; 3) the effects of MDD and age are positively correlated; 4) most genes that are age-dependent in control subjects display greater age effects in MDD subjects; and 5) the increased prevalence of age effects in MDD corresponds to similar trends in controls, rather than representing de novo age effects.