Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

[Objective]To investigate the non-suicidal self-injury(NSSI)behaviors in adolescents with depressive disorder,analyze related influencing factors,and provide theoretical basis and reference for the prevention and treatment of NSSI.[Methods]According to DSM-5 criteria,95 depressive adolescents were divided into two groups:one with NSSI(NSSI group)and one without NSSI(nNSSI group).All patients were assessed with Adolescent Non-suicidal Self-injury Assessment Questionnaire(ANSAQ),Self-Rating Depression Scale(SDS),Self-Rating Anxiety Scale(SAS),Simplified Coping Style Questionnaire(SCSQ),Experiences in Close Relationships-Relationship Structures Scale(ECR-RS),and Childhood Trauma Questionnaire-Short Form(CTQ-SF).The inter-group differences were compared.The influencing factors of NSSI were analyzed by using binary logistic regression.[Results]Of the 95 depressive adolescents,59 cases of NSSI were identified,with a detection rate of 62.11%.NSSI group had higher scores than nNSSI group on SDS,SAS,negative coping style,paternal attachment anxiety,maternal attachment anxiety and avoidance,CTQ-SF total score,emotional neglect,physical neglect,emotional abuse,and sexual abuse(all P<0.05).Binary logistic regression analysis showed that anxiety,negative coping style,maternal attachment avoidance and emotional abuse increased the risk of NSSI among adolescents with depressive disorders(all P<0.05).[Conclusions]Adolescents with depression have a high incidence of NSSI behaviors,which is related to anxiety,negative coping style,maternal attachment avoidance and emotional abuse.In addition to improving patients' depression and anxiety in clinical setting,attention should also be paid to patients' coping styles,parent-child relationship and childhood trauma to reduce the occurrence of NSSI behaviors.

The relationship between gut microbiota and depressive disorder has become a research focus in recent years. Within the microbiota-gut-brain axis, the gut microbiota influences the onset and progression of depressive disorder primarily through the tryptophan metabolic pathway. Tryptophan, an essential amino acid in humans, is subject to dual regulation by intestinal microorganisms, which modulate its metabolic balance via inflammatory stimulation and microbial metabolite production. In depression, excessive activation of the kynurenine branch of tryptophan metabolism leads to the accumulation of proinflammatory and neurotoxic metabolites, thereby exacerbating neuroinflammation in the brain. Intervention studies indicate that the antidepressant-like effects of probiotics and traditional Chinese medicine are associated with remodeling of the gut microbiota, restoration of tryptophan metabolic balance, and alleviation of neuroinflammation. Furthermore, targeted inhibition of kynurenine 3-monooxygenase can mitigate neuroinflammation by regulating microglial activity, thus improving depressive-like behaviors. In summary, the metabolite-inflammation axis represents a central node in the interaction regulation between tryptophan metabolism and the microbiota-gut-brain axis. This provides a theoretical foundation for developing novel therapeutic strategies targeting depression through modulation of gut microbiota-mediated tryptophan metabolism.
Tryptophan/metabolism* ; Gastrointestinal Microbiome/physiology* ; Humans ; Depressive Disorder/microbiology* ; Probiotics/therapeutic use* ; Brain/metabolism* ; Kynurenine/metabolism* ; Metabolic Networks and Pathways ; Animals ; Medicine, Chinese Traditional

Major depressive disorder is a common mental disorder,one of the core symptoms of which is anhedonia,characterized by a reduced ability to respond to pleasurable stimuli.Brain images of patients with major depressive disorders with anhedonia show the following features:reduced volume or cortical thickness in brain regions such as the striatum and temporal lobe,changes in the microstructure of white matter tracts,abnormal neuronal activity in the frontal lobe,temporal lobe,and limbic system,and altered connectivity in the default mode network,reward network,and fronto-parietal network.Additionally,factors such as stress,gene expression,the glutamate system,and biological rhythms may also influence anhedonia.The neurobiological mechanisms of anhedonia are intricate,and are crucial for the diagnosis,treatment,and prognosis of depressive disorders.

Major depressive disorder is a common mental disorder,one of the core symptoms of which is anhedonia,characterized by a reduced ability to respond to pleasurable stimuli.Brain images of patients with major depressive disorders with anhedonia show the following features:reduced volume or cortical thickness in brain regions such as the striatum and temporal lobe,changes in the microstructure of white matter tracts,abnormal neuronal activity in the frontal lobe,temporal lobe,and limbic system,and altered connectivity in the default mode network,reward network,and fronto-parietal network.Additionally,factors such as stress,gene expression,the glutamate system,and biological rhythms may also influence anhedonia.The neurobiological mechanisms of anhedonia are intricate,and are crucial for the diagnosis,treatment,and prognosis of depressive disorders.

Objective To investigate the changes in serum levels of claudin-5 and Apelin-13 in patients with depression and their relationship with disease progression and sleep disorders.Methods A total of 128 patients with depression admitted to our hospital from June 2021 to July 2023 were selected as the study group,and another 128 patients who underwent physical examinations during the same period were selected as the control group.The correlation between the expression levels of serum claudin-5 and Apelin-13 in patients with depression and the Hamilton Depression Rating Scale(HAMD)score,as well as the diagnostic value of serum claudin-5 and Apelin-13 for the severity of depression in patients were analyzed.Results The expression level of claudin-5 in the serum of patients in study group was higher than that of the control group,which increased with the severity of the disease(P<0.05)and was positively correlated with the HAMD score(r=0.713,P<0.05).In addition,the expression level of claudin-5 in the serum of patients with sleep disorders was higher than that of those without sleep disorders(P<0.05),and the trend of changes in the expression level of Apelin-13 was opposite;Age,age at onset of depression,and claudin-5 were factors for sleep disorders in patients with depression,while Apelin-13 was a protec-tive factor(P<0.05);The combined detection of serum claudin-5 and Apelin-13 is superior to their individual detection(Z combined detection-claudin-5=2.393,Z combined detection-Apelin-13=1.964,P=0.016,0.044).Conclusion The expression levels of claudin-5 and Apelin-13 in serum of patients with depression were related to the progression of disease and the sleep disorders and the combined detection has high diagnostic value for severe depression.