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.
Before paroxetine treatment, patients with the DRD2 A1+ allele (A1A2 genotype) compared to those with the A1- allele (A2A2 genotype) had higher total GHQ psychopathological scores (P=0.040) and higher GHQ subscale scores for anxiety/insomnia (0.046), social dysfunction (P=0.033) and depression (P=0.011).
In line with this, mice with varying 5-HTT genotypes are invaluable tools to study depression- and anxiety-like behaviours as well as the mechanisms mediating potential therapeutics.
Few studies of gene-environment interactions for the serotonin transporter promoter polymorphism (5-HTTLPR), life stressors and depression have considered women separately or examined specific types of stressful life events.
Since both posttraumatic stress disorder (PTSD) and depression are associated with disturbances in the serotoninergic system, the aim of the study was to determine the association between severity of PTSD symptoms, serotonin transporter polymorphism (5-HTTLPR) and platelet serotonin (5-HT) concentration, in male combat veterans with PTSD (n = 325), who were subdivided according to presence of comorbid depression.
In addition, we found two genes, SLC6A4 and SLC6A2, to be the main therapeutic targets, and Serotonin-Norepinephrine Reuptake Inhibitors (SNRI) and Tricyclic Antidepressants (TCA) to be the most effective drugs for individuals with depression at risk for suicide.
Additionally, to elucidate pathophysiological mechanisms that could explain the relations between MUPS and depression, we investigate the association between a sustained high level of MUPS, and (I) omega (ω)-3 and -6 fatty acid (FA)-status and (II) functional polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR).
Association of glucocorticoid and type 1 corticotropin-releasing hormone receptors gene variants and risk for depression during pregnancy and post-partum.
Initial conditions of psychotropic drug response: studies of serotonin transporter long promoter region (5-HTTLPR), serotonin transporter efficiency, cytokine and kinase gene expression relevant to depression and antidepressant outcome.
Additive effects of 5-HTTLPR (serotonin transporter) and tryptophan hydroxylase 2 G-703T gene polymorphisms on the clinical response to citalopram among children and adolescents with depression and anxiety disorders.
The association between the IL-6 polymorphism and reduced risk of depressive symptoms confirms the role of the inflammatory response system in the pathophysiology of IFN-alpha-induced depression; in contrast, the effect of the 5-HTT gene was small and perhaps dependent on the status of the inflammatory response.
5-HTTLPR genotype may also impact upon other regions of the brain, such as the OFC, but structural differences in these regions in early adolescence may not necessarily alter the risk for onset of depression during later adolescence.
Single nucleotide polymorphisms in the CRH receptor 1 (CRHR1) gene interact with ELS to predict depression, cognitive functions and hippocampal activity.
The severity of depression was assessed with the 21-item Hamilton Depression Rating scale, and the 5-HTTLPR genotypes in the patients were determined using the polymerase chain reaction.
Differential effects of DRN GR deletion in female mice may provide insight into the greater incidence of depression and specific depression symptoms in women.
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).
Previous studies have suggested that polymorphism in the serotonin transporter gene (5-HTTLPR) influences responses to serotonergic manipulation, with opposite effects in patients recovered from depression (rMDD) and controls.
In a 2-year prospective study of a community sample of 521 older people, information on number of physical disorders, diagnosis of depression (Geriatric Mental State), and genotypes for 6 pro-inflammatory (tumor necrosis factor-α -850C/T and -308G/A, interleukin (IL)-1β -511C/T and +3953C/T, IL-6-174G/C, IL-8 -251T/A) and 2 anti-inflammatory (IL-4 +33T/C, IL-10 -1082G/A) cytokine polymorphisms were ascertained.
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).
Several studies have demonstrated that variants of the CRH-R1 gene carry a potential risk for depression, but evidence for an association between CRH-R1 genotypes and IBS is lacking.
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.