“…In addition, CRP, a typical inflammatory factor, and whose levels can reflect the level of inflammation in the body, was not found to be increased in the present study, which is inconsistent with the findings of Howren et al. ( 31 ). The difference in the results of the above studies was considered to be due to the greater heterogeneity of MDD, as well as related to the fact that this study did not control for potential factors such as BMI and smoking.…”
ObjectiveThis study investigated the association between inflammatory cytokines and major depressive disorder.MethodsPlasma biomarkers were measured by enzyme-linked immunosorbent assay (ELISA). Statistical analysis of baseline biomarkers in the major depression disorder (MDD) group and healthy controls (HC) group, and differences in biomarkers before and after treatment. Spearman analysis was performed to correlate baseline and after treatment MDD biomarkers with the 17-item Hamilton Depression Rating Scale (HAMD-17) total scores. Receiver operator characteristic (ROC) curves were analyzed for the effect of biomarkers on MDD and HC classification and diagnosis.ResultsTumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were significantly higher in the MDD group than in the HC group, while high mobility group protein 1 (HMGB1) levels were significantly lower in the MDD group. The AUCs for HMGB1, TNF-α, and IL-6 were 0.375, 0.733, and 0.783, respectively, according to the ROC curves. MDD patients with brain-derived neurotrophic factor precursor (proBDNF) levels were positively correlated with total HAMD-17 scores. The levels of proBDNF levels were positively correlated with the total HAMD-17 score in male MDD patients, and brain-derived neurotrophic factor (BDNF) and interleukin 18 (IL-18) levels were negatively correlated with the total HAMD-17 score in female MDD patients.ConclusionInflammatory cytokines are associated with the severity of MDD, and TNF-α and IL-6 have the potential as objective biomarkers to aid in the diagnosis of MDD.
“…In addition, CRP, a typical inflammatory factor, and whose levels can reflect the level of inflammation in the body, was not found to be increased in the present study, which is inconsistent with the findings of Howren et al. ( 31 ). The difference in the results of the above studies was considered to be due to the greater heterogeneity of MDD, as well as related to the fact that this study did not control for potential factors such as BMI and smoking.…”
ObjectiveThis study investigated the association between inflammatory cytokines and major depressive disorder.MethodsPlasma biomarkers were measured by enzyme-linked immunosorbent assay (ELISA). Statistical analysis of baseline biomarkers in the major depression disorder (MDD) group and healthy controls (HC) group, and differences in biomarkers before and after treatment. Spearman analysis was performed to correlate baseline and after treatment MDD biomarkers with the 17-item Hamilton Depression Rating Scale (HAMD-17) total scores. Receiver operator characteristic (ROC) curves were analyzed for the effect of biomarkers on MDD and HC classification and diagnosis.ResultsTumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were significantly higher in the MDD group than in the HC group, while high mobility group protein 1 (HMGB1) levels were significantly lower in the MDD group. The AUCs for HMGB1, TNF-α, and IL-6 were 0.375, 0.733, and 0.783, respectively, according to the ROC curves. MDD patients with brain-derived neurotrophic factor precursor (proBDNF) levels were positively correlated with total HAMD-17 scores. The levels of proBDNF levels were positively correlated with the total HAMD-17 score in male MDD patients, and brain-derived neurotrophic factor (BDNF) and interleukin 18 (IL-18) levels were negatively correlated with the total HAMD-17 score in female MDD patients.ConclusionInflammatory cytokines are associated with the severity of MDD, and TNF-α and IL-6 have the potential as objective biomarkers to aid in the diagnosis of MDD.
“…Several studies have demonstrated that ECT can lead to a long‐term reduction in peripheral cytokine levels, 18–21 suggesting an anti‐inflammatory effect. However, more recent studies have shown that ECT did not significantly alter the peripheral blood concentrations of the inflammatory mediators in depressed patients 22–24 . In animal models, where electroconvulsive shock (ECS) is used to mimic the human intervention, the effects of ECS on central inflammation have not fully been disentangled either.…”
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confidence: 99%
“…However, more recent studies have shown that ECT did not significantly alter the peripheral blood concentrations of the inflammatory mediators in depressed patients. [22][23][24] In animal models, where electroconvulsive shock (ECS) is used to mimic the human intervention, the effects of ECS on central inflammation have not fully been disentangled either. Some studies have indicated that ECS can lead to astrocyte activation and an increase in inflammatory cytokines in the short term [25][26][27] ; however, these effects are rapid and may be transient.…”
AimThis study aimed to investigate the neuroinflammatory hypothesis of depression and the potential anti‐inflammatory effect of electroconvulsive therapy (ECT) in vivo, utilizing astrocyte‐derived extracellular vesicles (ADEVs) isolated from plasma.MethodsA total of 40 patients with treatment‐resistant depression (TRD) and 35 matched healthy controls (HCs) were recruited at baseline, and 34 TRD patients completed the post‐ECT visits. Blood samples were collected at baseline and post‐ECT. Plasma ADEVs were isolated and confirmed, and the concentrations of two astrocyte markers (glial fibrillary acidic protein (GFAP) and S100β), an EV marker cluster of differentiation (CD) 81, and nine inflammatory markers in ADEVs were measured as main analyses. Additionally, correlation analysis was conducted between clinical features and ADEV protein levels as exploratory analysis.ResultsAt baseline, the TRD group exhibited significantly higher levels of two astrocyte markers GFAP and S100β, as well as CD81 compared to the HCs. Inflammatory markers interferon (IFN)‐γ, interleukin (IL)‐1β, IL‐4, IL‐6, tumor necrosis factor (TNF)‐α, IL‐10, and IL‐17A were also significantly higher in the TRD group. After ECTs, there was a significant reduction in the levels of GFAP, S100β, and CD81, along with a significant decrease in the levels of IFN‐γ and IL‐4. Furthermore, higher levels of GFAP, S100β, CD81 and inflammatory cytokines were associated with more severe depressive symptoms and poorer cognitive function.ConclusionThis study provides direct insight supporting the astrocyte activation and neuroinflammatory hypothesis of depression using ADEVs. ECT may exert anti‐inflammatory effect through inhibition of such activation of astrocytes.This article is protected by copyright. All rights reserved.
“…The TyG index correlates positively with the levels of proinflammatory factors, such as leukocytes and C‐reactive protein, which correlate positively with the severity of depression. Antidepressants can reduce the levels of proinflammatory factors in patients with depression 42,43 . The fourth factor is oxidative stress.…”
Section: Discussionmentioning
confidence: 99%
“…Antidepressants can reduce the levels of proinflammatory factors in patients with depression. 42,43 The fourth factor is oxidative stress. Brain tissue is extremely high in oxygen consumption and has weak antioxidant capacity.…”
Growing evidence suggests that hypertensive individuals have a greater risk of developing depression, and depression can also increase the incidence of hypertension. In the hypertensive population, the association between triglyceride glucose (TyG) index and depression remains unclear. This study aimed to assess the association between TyG index and depression in hypertensive people through the cross‐sectional study of the National Health and Nutrition Examination Survey (2007–2018). To assess the relationship between TyG index and depression in hypertensive population, we conducted weighted multiple logistic regression models and used a generalized additive model to probe for nonlinear correlations. In addition, we employed a recursive algorithm to determine the inflection point and established a two‐piece linear regression model. This study enrolled 5897 individuals. In the model adjusted for all covariates, the ORs (95% CI) for the relationship between TyG index and depression in hypertensive population were 1.32 (1.12–1.54). A nonlinear association was found between TyG index and depression, with an inflection point at 8.7. After the inflection point, the ORs (95% CI) were 1.44 (1.15–1.79). Only the interaction with the obese population was statistically significant. Our study highlighted a nonlinear association between TyG index and depression in American hypertensive adults.
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