Ligands and receptors of the TNF superfamily are decreased in major depression and during early antidepressant therapy

Schmidt, F.; Koch, Jenny; Nowak, C. N.; Holdt, Lesca M.; Teupser, Daniel; Hegerl, Ulrich; Himmerich, Hubertus

doi:10.1016/j.jpsychires.2019.09.010

Cited by 24 publications

(22 citation statements)

References 53 publications

(64 reference statements)

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“…Neither has it been explored whether low sTWEAK, high galectin-3, high HbA1c and low HDL-cholesterol were independently associated with depression. We only found one previous study exploring the association between sTWEAK and depression, and that study was performed in a population without diabetes [14]. Their findings of an association between low sTWEAK levels and depression is in accordance with our findings.…”

Section: Discussionsupporting

confidence: 92%

“…High levels of sTWEAK are released by normal arteries, but are diminished in people with chronic vascular damage such as carotid stenosis, coronary artery disease and heart failure [8,9], resulting in an increased risk for CV mortality [10]. Low sTWEAK levels have been demonstrated in people with T1D [11], type 2 diabetes (T2D) [12], gestational diabetes [13], depression [14], and in people with bipolar disorder during ongoing manic episodes [15].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

Melin

Dereke

Hillman

2019

Preprint

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BackgroundLow levels of soluble TNF-like weak inducer of apoptosis (sTWEAK) have previously been linked to cardiovascular disease, which is also the case for depression. High levels of galectin-3 and HbA1c, and low levels of HDL-cholesterol, have previously been linked to depression in these patients. The aim was to explore whether low levels of sTWEAK were associated with depression in type 1 diabetes patients. We adjusted for age, sex, galectin-3, HbA1c, HDL-cholesterol, antidepressants, and cardiovascular complications. MethodsCross-sectional design. Type 1 diabetes patients (n=287, men 56%, age18-59 years) were consecutively recruited from one specialist diabetes out-patient clinic. Depression was defined as Hospital Anxiety and Depression Scale-Depression sub scale ≥8 points. Blood samples, anthropometrics and blood pressure were collected, supplemented with data from electronic medical records. ELISA was used to measure sTWEAK and galectin-3. Low sTWEAK was defined as <7.1 ng/ml (<70th percentile), high galectin-3 as ≥2.562 µg/l (≥85th percentile) and high HbA1c as >70 mmol/mol (>8.6%). Non-parametric tests were used. Multiple logistic regression analyses (Backward: Wald) were performed, and calibrated and validated for goodness of fit with the data variables. Results Median (q1, q3) (ng/ml) sTWEAK were for 30 depressed and 257 non-depressed patients 1.5 (1.2, 2.9) and 2.7 (1.3, 13.0) respectively (p =0.021); median (q1, q3) (µg/l) galectin-3 were 1.348 (0.827, 2.850) and 0.916 (0.533, 1.637) respectively (p = 0.005). Four-teen percent of patients with low sTWEAK were depressed, and 2% of patients with high sTWEAK were depressed (p = 0.003). Low sTWEAK (adjusted odds ratio (AOR) (CI)) 9.5 (2.0-46) ), high galectin-3 (AOR (CI) 6.5 (2.3-18.7)), use of antidepressants (AOR (CI) 10.3 (3.3-30.4)), HDL-cholesterol (per mmol/l) (inversely) (AOR (CI) 0.1 (0.03-0.5)), and age (per year) (AOR (CI) 1.05 (1.00-1.09)) were associated with depression. ConclusionsThe depressed patients with type 1 diabetes had lower levels of sTWEAK than the non-depressed, which might contribute to the increased risk for cardiovascular disease and mortality previously demonstrated in patients with depression. Low levels of sTWEAK and HDL-cholesterol and high levels of galectin-3 were independently associated with depression.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

Melin

Dereke

Hillman

2019

Preprint

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“…33 To date, circulating TWEAK concentrations have only been investigated in mental disorders such as major depression, bipolar disorder and crack cocaine dependence. [23][24][25][26] The major depression study found that serum TWEAK levels were lower in both unmedicated and medicated depression patients than healthy controls. 26 Regarding bipolar disorder, Barbosa et al 23 found a link between higher TWEAK concentrations and bipolar disorder, concluding that TWEAK may play a role in the pathophysiology of bipolar disorder.…”

Section: Discussionmentioning

confidence: 99%

“…[20][21][22] In addition, TWEAK has been studied in connection with psychiatric disorders, such as major depression, bipolar disorder, cocaine dependence. [23][24][25][26] To the best of our knowledge, only one study has investigated TWEAK levels in schizophrenia. 27 Given the importance of neuroinflammation changes in schizophrenia, biomarkers of persistent inflammation are needed, especially in view of therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Serum tumor necrosis factor-like weak inducer of apoptosis levels are elevated in schizophrenia

Kılıç

Işık

Usta

et al. 2021

Braz. J. Psychiatry

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The purpose of this study was to assess serum Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) concentrations to determine whether changes in patients with schizophrenia could have etiopathogenetic importance. Since very little research has addressed the connection between the inflammatory marker TWEAK and schizophrenia, we wanted to examine alterations of TWEAK and investigate the possible correlation between clinical symptomatology and serum concentrations. Methods: A total of 45 schizophrenia patients and 40 healthy controls were included in this study. The Positive Symptom Assessment scale and the Negative Symptom Assessment scale were administered to determine symptom severity. Venous blood samples were collected and serum TWEAK levels were measured. Results: Serum TWEAK levels were significantly higher in the schizophrenia group than the control group, independently of potential confounders, including sex, age, body mass index and smoking status. Conclusion: The results indicate that TWEAK is elevated in schizophrenia patients, which could deepen our understanding of the role of inflammation in the pathogenesis of schizophrenia.

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“…The S/S genotype in this region is associated with decreased serotonin expression and increased susceptibility to depression [12]. TNF and IL-1B may be involved in major depression not just by activating certain cascades of in ammation but by many other mechanisms [24]. It is not di cult to see that ginseng's treatment of depression involves neurotransmitters (especially serotonin), in ammation, neurotrophic factors and many other aspects.…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology-based active compounds and pharmacological mechanisms of ginseng for depression in post-COVID-19

Wang

et al. 2020

Preprint

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Abstract Introduction: The novel coronavirus disease 2019 (COVID-19) is in the midst of worldwide panic. Sudden onset of an immediate life-threatening illness, quarantine and unemployment caused by epidemic are all contributors to depression. Ginseng has been reported to be an effective and safe clinical treatment on both immune-regulation and anti-depression. However, the mechanism of its anti-depression effect has not been fully characterized. In order to provide theoretical guidance for further clinical application in post-pandemic, we investigated active compounds and pharmacological mechanisms of ginseng to exert anti-depressant activity using network pharmacology, and discussed the active ingredients with immune-regulation and anti-depression.Methods: Information on compounds in ginseng was obtained from public databases, and genes related to depression were gathered using the GeneCards database. Networks of ginseng-associated targets and depression-related genes were constructed through STRING database. Potential targets and pathway enrichment analysis related to the therapeutic efficacy of ginseng for depression were identified using Cytoscape and Database for Annotation, Visualization and Integrated Discovery (DAVID). Results: Network pharmacological analysis of ginseng in treatment of depression identified 16 active ingredients, 47 potential targets, 32 GO terms, and 8 target gene-regulated major pathways. Among them, kaempferol, beta-sitosterol, stigmasterol, fumarine and frutinone A are bioactive compounds and key chemicals. Core genes in PPI network were AKT1, CASP3, NOS3, TNF, and PPARG. Enrichment results revealed that ginseng could regulate multiple aspects of depression through neuroactive ligand-receptor interaction, HIF-1 signaling pathway, and Serotonergic synapse. More importantly, we found that frutinone A and kaempferol are key ingredients in ginseng with dual activities of immune-regulation and anti-depression. Conclusions: We discovered that the therapeutic activities of ginseng for depression mainly involve neurotransmitters, neurotrophic factors, neurogenesis, HPA axis and inflammatory response. Pharmacological network analysis can help to explain the potential effects of ginseng for treating depression, indicating that ginseng is a preferable herb clinically for immune-regulation and anti-depression in post-pandemic.

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Ligands and receptors of the TNF superfamily are decreased in major depression and during early antidepressant therapy

Cited by 24 publications

References 53 publications

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

Serum tumor necrosis factor-like weak inducer of apoptosis levels are elevated in schizophrenia

Network pharmacology-based active compounds and pharmacological mechanisms of ginseng for depression in post-COVID-19

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