Selective serotonin reuptake inhibitors (SSRIs), such as citalopram, which selectively block serotonin transporter (5-HTT) activity, are widely used in the treatment of depression and anxiety disorders.
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.
The aim of this study is to investigate the development of depression during interferon-alpha (IFN-α) therapy and the variations in the expression of the serotonin receptor (5-HTR) and transporter (5-HTT) in hepatitis C patients.
Our investigation suggested that the increased expression of 5HTT mRNA in peripheral leukocytes may be related with the pathophysiology of depression and its reduction after treatment may reflect the adaptive change induced by the antidepressant.
These observations demonstrate that IL6 directly controls SERT levels and consequently serotonin reuptake and identify STAT3-dependent regulation of SERT as conceivable neurobiological substrate for the involvement of IL6 in depression.
The aims of this study were (1) to investigate the association between 5HTT methylation or expression in leukocytes and depression and (2) to investigate a possible effect of 5HTT methylation, expression, and genotype on clinical symptoms in MDD.
Several behavior tests (sucrose preference test (SPT), forced swimming test (FST) and tail suspension test (TST)) and biochemical parameters (IL-6, TNF-α and SOD levels) were used to evaluate the antidepressive effect of PF on LPS-induced depression model.
The factors that most strongly influenced changes in serum BDNF levels following treatment in an alcohol detoxification program were variants of the BDNF gene and ongoing depression.
Using BDNF knockdown by RNA interference and lentiviral vectors injected into specific subregions of the hippocampus we show that a reduction in BDNF expression in the dentate gyrus, but not the CA3, reduces neurogenesis and affects behaviors associated with depression.
In addition, six glucocorticoid receptor pathway genes (Slc22a5, Aqp1, Stat5a, Ampd3, Plekhf1, and Cyb561) were upregulated in GF mice, and of these only two (Stat5a and Ampd3) were upregulated in LPS-treated mice, whereas the shared gene, Stat5a, was downregulated in "depression microbiota" recipient mice.
We conclude that BH<sub>4</sub> treatment of HPA toward systemic L-Phe lowering reverses elevated brain L-Phe content but the recovery of TPH2 protein and activity as well as serotonin levels is suboptimal, indicating that patients with mild HPA and mood problems (depression or anxiety) treated with the current diet may benefit from supplementation with BH<sub>4</sub> and 5-OH-tryptophan.
The aim of this study was to investigate the effects of probiotic and synbiotic supplementation on the depression and anxiety symptoms and serum brain-derived neurotrophic factor (BDNF) level.
At the molecular level, the expression of Brain-Derived Neurotrophic Factor (BDNF), a neuropeptide associated with depression, and few other stress-specific genes CRH, NR3C1, CART, and NPY were measured in the Prefrontal Cortex (PFC) region of the reward circuitry.
Interestingly, the depression-associated module was highly enriched for pathways related to immune function and was also associated with TL and IL-6 cytokine levels.