However, very few studies have so far focused on the degree to which rare variants of SLC6A4 are responsible for the depression observed in adolescent and young adult suicide patients.
The S allele of 5-HTTLPR combined with exposure to childhood adversity or a poorer parenting environment was associated with a smaller hippocampal volume and subsequent onset of depression.
Over-representation of the LL genotype of the 5-HTTLPR and higher platelet 5-HT concentrations were detected in veterans with PTSD who did not develop comorbid depression but had severe early insomnia.
Antidepressants that block the serotonin transporter, (Slc6a4/SERT), selective serotonin reuptake inhibitors (SSRIs) improve mood in adults but have paradoxical long-term effects when administered during perinatal periods, increasing the risk to develop anxiety and depression.
The present study investigated the association of 5-HTTLPR polymorphism and CpG DNA methylation (5mC) levels of an AluJb repeat element at the SLC6A4 promoter region in mother-child pairs exposed to maternal depression.
Two independent longitudinal studies (n = 681 and 176, respectively) examined whether 5-HTTLPR moderated associations between low levels of positive parenting at 11-13 years and subsequent depression at 17-19 years.
Increasing evidence have indicated the strong association of stress, especially the chronic stress and early life stress, with depressive disorders development, while the association of stress with depression is moderated by genetic risk factors, including polymorphism of SERT, BDNF, GR, FKBP5, MR, and CRHR1.
We found that the association between SLE load and MS depression severity was stronger among those with one or two copies of the short allele of the 5-HTTLPR.
In humans, the short allele of a common polymorphism in the serotonin transporter (5-HTT) gene is associated with a higher risk to develop depression and anxiety disorders.
The serotonin transporter (SERT) gene has been linked to depression, especially the short allele of the serotonin transporter linked polymorphic region (5-HTTLPR).
Results showed a small but significant effect of 5-HTTLPR in interaction with stress in the prediction of depression (OR[95%CI] = 1.18[1.09; 1.28], n = 48 effect sizes from 51 studies, totaling 51,449 participants).
The aim of the present conceptual replication study was to investigate the role of biased automatic approach-avoidance tendencies as a candidate intermediate phenotype for depression, in the context of genes (5-HTTLPR polymorphism) and childhood trauma.
The aim of this study was to determine whether genetic variation in the SLC6A4 gene influences promoter DNA methylation, and whether these are associated with depression status.
Here we examined whether emotional inertia, the tendency for a person's emotions to carry over from 1 moment to the next and a prospective predictor of the development of depression, is associated with a known genetic risk factor for emotional dysregulation, a polymorphism in the serotonin transporter gene (5-HTTLPR).
The S allele of serotonin transporter gene (5-HTTLPR) has been found to increase the risk of depression and other mental health problems, but some evidence suggests that S-allele carriers outperform subjects carrying the long allele in an array of cognitive tasks.
A number of studies have shown that the presence of short (S) allele of the serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with a higher risk for depression following exposure to stressful life events.
Additionally, we found no relationship between pretreatment amygdala binding and posttreatment depression score, and were unable to predict posttreatment depression severity using both pretreatment 5-HTT (in the amygdala) and 5-HT<sub>1A</sub> binding (in the raphe).
Amitifadine, the only drug ever clinically tested in Phase 3 for treating depression, is a triple reuptake inhibitor (TRI) that simultaneously interacts with human monoamine transporters (MATs) including hSERT, hNET and hDAT.