scholarly journals Tumor Necrosis Factor-α Variations in Patients With Major Depressive Disorder Before and After Antidepressant Treatment

2020 ◽  
Vol 11 ◽  
Author(s):  
Lin Yao ◽  
LiHong Pan ◽  
Min Qian ◽  
Wei Sun ◽  
ChunHong Gu ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Tumor Necrosis Factor ◽  
Depressive Disorder ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Antidepressant Treatment ◽  
Major Depressive ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) had been identified as a key pro-inflammatory cytokine in the pathophysiology of major depressive disorder (MDD) and the mechanism of antidepressant treatment. The primary aim of the present study was to examine the serum TNF-α levels in Chinese inpatients with MDD during the acute phase and to explore the changes in TNF-α levels after effective clinical treatment. Fifty-seven consecutive inpatients with MDD and 30 healthy controls were recruited. The serum TNF-α levels were detected using ELISA. Symptoms of depression were evaluated using the 24-item Hamilton Rating Scale for Depression (HAM-D-24). TNF-α levels and HAM-D-24 scores were assessed at baseline and after 2 and 12 weeks of follow-up. The serum TNF-α levels were higher in the MDD group than in the control group. After 2 and 12 weeks of antidepressant treatment, there were significant improvements in the patients' symptoms and significant decreases in the TNF-α levels. The baseline TNF-α levels significantly correlated with the decreased HAM-D-24 scores, particularly for the depressive symptoms of anxiety/somatization and weight loss. The present findings indicate that depression is accompanied by activation of TNF-α, which also has a predictive value for the antidepressant treatment response in patients with MDD.

scholarly journals Increased soluble tumor necrosis factor-α receptors in patients with major depressive disorder

2009 ◽  
Vol 63 (2) ◽  
pp. 202-208 ◽  
Author(s):  
Rodrigo Grassi-Oliveira ◽  
Elisa Brietzke ◽  
Júlio C. Pezzi ◽  
Rodrigo P. Lopes ◽  
Antonio L. Teixeira ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Tumor Necrosis Factor ◽  
Depressive Disorder ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Major Depressive ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Low tumor necrosis factor-α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder

2018 ◽  
Vol 8 (4) ◽  
pp. e00933 ◽  
Author(s):  
Annamari Sorri ◽  
Kaija Järventausta ◽  
Olli Kampman ◽  
Kai Lehtimäki ◽  
Minna Björkqvist ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Tumor Necrosis Factor ◽  
Depressive Disorder ◽  
Electroconvulsive Therapy ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Symptom Reduction ◽  
Major Depressive ◽  
Factor Α ◽  
Necrosis Factor

Associations of Tumor Necrosis Factor–α G-308A (rs1800629) Gene Polymorphisms with Major Depressive Disorder

2021 ◽  
Vol 19 (7) ◽  
pp. 133-136
Author(s):  
Aamal Muhsen Kadhum ◽  
Bayader M. Abd Al–Kadim ◽  
Thanaa Chasib Kareem ◽  
Ali Ahmed Nayyef ◽  
Mona N. Al-Terehi
Keyword(s):  
Major Depressive Disorder ◽  
Tumor Necrosis Factor ◽  
Depressive Disorder ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Control Group ◽  
Major Depressive ◽  
Allele Distribution ◽  
Tnf Α ◽  
Necrosis Factor

Pro-inflammatory cytokine polymorphisms like Tumor Necrosis Factor- (TNF), has been found associated to severe depressive disorder (MDD). The Pro-inflammatory cytokines tumor necrosis factor (TNF-α) G-308A (rs1800629) have been discovered to have an important role in the pathophysiology of depressive disorders and the mechanism of antidepressant treatment. The present study aims to study TNF-α gene polymorphisms in Major depressive disorder using allele specific PCR. The results show that family history are non- significant different between patients and control group (0.6346) and also there was non- significant different in BMI (0.3417), The genotyping data show tow alleles and three genotyping (AG, GG, AA) the statically analysis show non-significant differences between patients and controls groups (0.095, 0.800) for GG, AA and GA respectively with more frequent of GA in patients than control group, the G allele was less frequent in patient than control while A allele was more frequent in patients than control group in significant differences (0.0001). It can be concluded that TNF genotyping didn’t impact in the Major depressive disorder but the allele distribution may have potential role in MDD patients.

scholarly journals Serum Levels of Tumor Necrosis Factor-α and Loudness Dependence of Auditory Evoked Potentials at Pretreatment and Posttreatment in Patients with Major Depressive Disorder

2019 ◽  
Vol 9 (10) ◽  
pp. 253
Author(s):  
Bun-Hee Lee ◽  
Young-Min Park ◽  
Seung-Hwan Lee ◽  
Miseon Shim
Keyword(s):  
Major Depressive Disorder ◽  
Tumor Necrosis Factor ◽  
Depressive Disorder ◽  
Tumor Necrosis ◽  
Auditory Evoked Potentials ◽  
Major Depressive ◽  
Tnf Α ◽  
Loudness Dependence ◽  
Α Level ◽  
Necrosis Factor

Background: Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), are associated with the pathophysiology of major depressive disorder (MDD). Several studies have reported that increased TNF-α might be associated with tryptophan depletion, which eventually could result in MDD. However, other studies revealed that TNF-α increased serotonin firing in raphe. Therefore, whether TNF-α increases or decreases serotonin activity remains unclear. Here, we aimed to determine the relationship between serum TNF-α level and central serotonergic activity using the loudness dependence of auditory evoked potentials (LDAEP) and standardized low-resolution brain electromagnetic tomography (sLORETA), as well as to evaluate the effects of antidepressants on TNF-α levels. Methods: LDAEP, serum TNF-α level, and depression severity were measured in 64 MDD outpatients pre and post 3 months of treatment. Results: Pretreatment TNF-α levels were negatively correlated with the pretreatment N1 sLORETA-LDAEP, P2 sLORETA-LDAEP, and N1/P2 sLORETA-LDAEP (p < 0.05). In multiple regression analysis for N1/P2 sLORETA-LDAEP, lower N1/P2 sLORETA-LDAEP was significantly related to higher TNF-α (CE = −0.047, p = 0.017) when all subjects were dichotomized based on the median TNF-α level (7.16 pg/mL) into pretreatment low- and high-TNF-α groups. In addition, the pretreatment Beck Depression Inventory, P2 LDAEP, and N1/P2 sLORETA-LDAEP were greater in the high-TNF-α groups than in the low-TNF-α groups (p < 0.05). Moreover, the posttreatment TNF-α level was significantly decreased compared to the pretreatment TNF-α level (z = −2.581, p = 0.01). However, the posttreatment TNF-α levels were not associated with posttreatment LDAEP. Conclusions: Higher TNF-α level is associated with decreased LDAEP, which could indicate compensatory elevation of central serotonin activity in outpatients with MDD, although this effect disappeared and TNF-α level was reduced after three months of antidepressant treatment.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor α Inhibition for Alzheimer’s Disease

2017 ◽  
Vol 9 ◽  
pp. 117957351770927 ◽  
Author(s):  
Rudy Chang ◽  
Kei-Lwun Yee ◽  
Rachita K Sumbria
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Short Review ◽  
Tnf Α ◽  
Factor Α ◽  
Ad Therapy ◽  
Necrosis Factor

Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.

Tumor necrosis factor-α-associated lysosomal permeabilization is cathepsin B dependent

2002 ◽  
Vol 283 (4) ◽  
pp. G947-G956 ◽  
Author(s):  
Nathan W. Werneburg ◽  
M. Eugenia Guicciardi ◽  
Steven F. Bronk ◽  
Gregory J. Gores
Keyword(s):  
Tumor Necrosis Factor ◽  
Cathepsin B ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fluorescent Protein ◽  
Tnf Α ◽  
Calcein Release ◽  
Green Fluorescent ◽  
Factor Α ◽  
Necrosis Factor

Cathepsin B (Cat B) is released from lysososomes during tumor necrosis factor-α (TNF-α) cytotoxic signaling in hepatocytes and contributes to cell death. Sphingosine has recently been implicated in lysosomal permeabilization and is increased in the liver by TNF-α. Thus the aims of this study were to examine the mechanisms involved in TNF-α-associated lysosomal permeabilization, especially the role of sphingosine. Confocal microscopy demonstrated Cat B-green fluorescent protein and LysoTracker Red were both released from lysosomes after treatment of McNtcp.24 cells with TNF-α/actinomycin D, a finding compatible with lysosomal destabilization. In contrast, endosomes labeled with Texas Red dextran remained intact, suggesting lysosomes were specifically targeted for permeabilization. LysoTracker Red was released from lysosomes in hepatocytes treated with TNF-α or sphingosine in Cat B(+/+) but not Cat B(−/−) hepatocytes, as assessed by a fluorescence-based assay. With the use of a calcein release assay in isolated lysosomes, sphingosine permeabilized liver lysosomes isolated from Cat B(+/+) but not Cat B(−/−) liver. C6ceramide did not permeabilize lysosomes. In conclusion, these data implicate a sphingosine-Cat B interaction inducing lysosomal destabilization during TNF-α cytotoxic signaling.

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