The estrogen receptor (ER) mechanisms by which 17β-estradiol influences depressive-like behaviour have primarily been investigated acutely and not within an animal model of depression.
Our findings suggest that in MDD, immune activation is associated with a simultaneous activation of dynorphin/KOR and β-endorphin/MOR signaling and that these opioid systems may participate in the pathophysiology of depression by a) exerting immune regulatory activities attenuating the primary immune response; and b) modulating reward responses and mood as well as emotional and behavioral responses to stress.
The aim of this study was to determine the effectiveness of CYP2D6 pharmacogenetic screening to accelerate drug dosing in older patients with depression initiating nortriptyline or venlafaxine.
182 subjects diagnosed with depression and treated with these drugs were clinically and therapeutically characterized and submitted to the quantification of drug/metabolite plasma concentrations and genotyping of ABCB1, CYP2C9, CYP2C19, and CYP2D6 genes.
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.
Then, we analyzed the expression of NET correlation with inflammatory cytokines to provide a new direction for detecting the association mechanism between depression and hypertension.
182 subjects diagnosed with depression and treated with these drugs were clinically and therapeutically characterized and submitted to the quantification of drug/metabolite plasma concentrations and genotyping of ABCB1, CYP2C9, CYP2C19, and CYP2D6 genes.
A search strategy was developed using the terms: "Mood disorder" OR "Depressive Disorder" OR "Bipolar disorder" AND "Infliximab" OR "tumor necrosis factor antagonist" as text words and Medical Subject Headings (i.e., MeSH and EMTREE).
In comparison with other biologics, patients receiving etanercept appeared to have a lower risk of depression.Key Points• Rheumatoid arthritis patients possessed higher risk of depression and anxiety.• Both depression and anxiety are strongly correlated with the subjective components of DAS28-ESR.• Etanercept might be the choice of biologics in rheumatoid arthritis patients with depression.
The objective of this study was to report long-lasting effects of bupropion on brain dopamine transporter (DAT) in a patient with depression and parkinsonism.
Brain-derived neurotropic factor (BDNF), a neurotrophic factor, plays important regulatory roles in depression by its high-affinity tropomysin-related kinase B (TrkB) receptor.
In addition, NR decreased the number of activated microglia in the hippocampus, and it reduced the levels of pro-inflammatory (IL-1β, IL-6, and TNF-α) and anti-inflammatory (IL-10 and TGF-β) cytokines in the brain of mice with alcohol-induced depression.
The hippocampus is particularly vulnerable to altered concentrations of the pro-inflammatory cytokine interleukin-1β (IL-1β), with elevated levels implicated in the aetiology of neurodegenerative disorders such as Alzheimer's and Parkinson's, and stress-related disorders such as depression.
Synaptic transmission efficacy can be bi-directionally modified through potentiation (long-term potentiation (LTP)) or depression (long-term depression (LTD)) as well as the phosphorylation state of Ser831 and Ser845 sites at the GluA1 subunit of the glutamate AMPA receptors, which has been characterized as a critical event for this synaptic plasticity.
The specific aim of this study was to explore the relationships between biomarkers of neural health: nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), immune health: interleukin 6 (IL-6), c-reactive protein (CRP), and cortisol, as well as the presence of depression, in physically active cannabis users (CU) and non-users (NU).
182 subjects diagnosed with depression and treated with these drugs were clinically and therapeutically characterized and submitted to the quantification of drug/metabolite plasma concentrations and genotyping of ABCB1, CYP2C9, CYP2C19, and CYP2D6 genes.
The Mini-BESTest score was lower in patients with lower serum hemoglobin (r = 0.396, p = 0.001) and albumin levels (r = 0.440, p < 0.001), severe disease-related symptoms (r = - 0.39, p = 0.02), and depression (r = - 0.538, p < 0.001).
Taken together our data indicate for first time that increased expression of A<sub>1</sub>R and Homer1a in the hippocampus modulates the resilience to stress-induced depression and thus might potentially mediate the detrimental effects of chronic sleep restriction on mood.
This study aimed to assess whether HSD11B1 genotypes and haplotypes are associated with depression risk, severity of symptoms and suicidal attempts, considering early-life stress as an environmental factor.
This study provides evidence that fluoxetine is a potent enhancer of GAP-43, a protein related to the neuronal plasticity, in the hippocampus of the rat model of depression.
This study further confirms that the imbalance between proBDNF/p75NTR/sortilin and mBDNF/TrkB production is important in the pathogenesis of depression.