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.
Our studies demonstrated that CGA pretreatment ameliorated depression-like behavior (SPT, FST, TST, and OFT) and serum biochemical levels (5-HT, DA, IL-6, and TNF-α) in ACTH-induced depression rats.
Stress-related suppression of TNFα predicted drinking severity only in alcohol-dependent individuals with subclinical depression, and suppressed TNFR1 following stress was only seen in individuals with subclinical depression.
The results showed that there were different levels of depression in patients with ovarian cancer in II~III stage, and the degree of depression could stimulate the level of serum-6, and TNF -α in serum increased.
To further elucidate inflammatory mechanisms related to TNF in depression, the aim of the current study was to investigate the involvement of ligands and receptors of the TNF/TNF-receptor-superfamily yet un- or little explored in major depression.
Since depression is a common co-morbid condition with PD, we undertook this study to determine whether Hc-TeTx might also show antidepressant-like properties and whether central brain-derived neurotrophic factor (BDNF) and/or tumor necrosis factor (TNF)-alpha are also affected by it.
Considering the inflammatory-depression link, and that women are twice as likely to experience depression compared to men, the current study (<i>N</i> = 475 university students) examined the moderating role of three independent cytokine single nucleotide polymorphisms (SNPs; IL-1β rs16944, IL-6 rs1800795 SNP, TNF-αrs1800629) in the relationship between early-life adversity and depressive symptoms, and whether these relations differed between males and females.
These results suggest a complex role for TNF-based neuroinflammation in SCI-induced depression that needs to be further explored, perhaps in conjunction with a broader targeting of additional post-SCI inflammatory cytokines.
The biological link between depression, inflammation, and CVD can be related to high levels of pro-inflammatory cytokines, such as IL-1β, TNF-α, and IL-6, released by macrophages which play a central role in the pathophysiology of both depression and CVD.
We estimated seven regularized Mixed Graphical Models in the Netherlands Study of Depression and Anxiety (NESDA) data (N = 2321) to explore shared variances among (1) depression severity, modeled via depression sum-score, nine DSM-5 symptoms, or 28 individual depressive symptoms; (2) inflammatory markers C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α); (3) before and after adjusting for sex, age, body mass index (BMI), exercise, smoking, alcohol, and chronic diseases.
This review outlines the immunological mechanism of T1D and depression, with a particular emphasis on the role of tumor necrosis factor-<i>α</i> (TNF-<i>α</i>), IL-1<i>β</i>, and interferon-<i>γ</i> (IFN-<i>γ</i>) cytokines and their signaling pathways.
We assessed trauma exposure, PTSD and depression severity, and quantified a panel of pro- inflammatory cytokines, including interleukin (IL)-1β, IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), interferon ϒ (IFN<sub>ϒ</sub>), and anti-inflammatory cytokines, including IL-4, IL-10 and IL-13 with enzyme-linked immunosorbent assays.
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 finding that FLX improved depressive behavior and pain through normalized 5-HT concentrations and TNF-α mRNA expression establishes the initial mechanism of the comorbidity of pain and depression.
According to the current literature, it seems that peripheral levels of interleukin (IL)-6, IL-10, IL-12, IL-13, and tumor necrosis factor (TNF)-α are elevated and that interferon (IFN)-γ levels are lower in patients with depression compared to healthy controls.
To gain rich and valid information at the symptom level, this article developed a depression test under the framework of cognitive diagnosis models (CDMs), referred to as CDMs-D. A total of 1,181 individuals were finally recruited and their responses were used to examine the psychometric properties of CDMs-D. After excluding poor items for statistical reasons (e.g., low discrimination, poor model-fit or having DIF), 56 items were included in the CDMs-D.
We undertook this study to determine whether MOX would actually show antidepressant-like properties in an animal model of depression and whether it would affect the hippocampal and frontal cortex levels of brain-derived neurotrophic factor (BDNF) or tumor necrosis factor (TNF)-alpha, peptides that have been implicated in pathogenesis of depression and effectiveness of various antidepressants.
1 L-1β, TNF-α and COX-2), increased BDNF expression and neurogenesis, restored the dysfunction of ATP production and oxidative stress in inflammation- induced depression.
There was a significant difference in the TNF-α levels between the subjects with and without restless legs symptoms in the depression group (p < .001) and among the patients with depressive symptoms but no a depression diagnosis (p = .022).