Yiming Wang

Background: Major depressive disorder (MDD) in adolescence is characterized by high prevalence (24.3% in China) and social dysfunction, particularly in competitive and cooperative behaviors. This study used fNIRS hyperscanning to explore cortical connectivity alterations during parent–adolescent interactions in adolescent MDD. Methods: Thirty‐three MDD adolescents (DD) and 29 healthy controls (HCs) completed competitive/cooperative maze tasks with parents under 52‐channel fNIRS. Wavelet coherence analyzed functional connectivity (FC) in prefrontal/motor regions, which provides undirected connectivity estimates. Group × task effects were tested via GLMM and FDR correction. Results: (1) Competition: DD exhibited hyperconnectivity in emotion regulation circuits between right opercular inferior frontal gyrus and left triangular inferior frontal gyrus (rIFGoperc and lIFGtriang, p = 0.047) but hypoconnectivity in executive networks between left dorsal superior frontal gyrus and left precentral gyrus (lSFGdor and lPreCG, p = 0.040). (2) Cooperation: DD showed enhanced motor–cognitive integration between right supplementary motor area and right middle frontal gyrus (rSMA and rMFG, p = 0.036) but impaired socioemotional processing between right triangular inferior frontal gyrus and left dorsal superior frontal gyrus (rIFGtriang and lSFGdor, p = 0.033). Task modulation: Within DD, cooperation preferentially engaged emotional resonance networks between right inferior orbital frontal gyrus and right medial superior frontal gyrus (rORBinf and rSFGmed, p = 0.031) while competition was associated with enhanced coupling in self‐monitoring circuits between left dorsal superior frontal gyrus and right opercular inferior frontal gyrus (lSFGdor and rIFGoperc, p = 0.047). Conclusions: Adolescent MDD involves context‐dependent neural deficits in social cognition, suggesting targets for neuromodulatory interventions.

Objective: Depression may be accompanied by cognitive impairment, but its pathogenesis remains unclear. This study aims to investigate the protective effects of fluoxetine on behavioral performance and prefrontal cortex neuronal damage in rats with depression-associated cognitive impairment, based on the observation of VGLUT2 protein expression.Methods: Forty-five SPF-grade male SD rats were randomly divided into three groups (n = 15): normal control group (CON), depression group (DD), and fluoxetine group (DD + F). The CON group was reared normally, while the DD and DD + F groups underwent chronic unpredictable mild stress (CUMS) combined with social isolation to induce a depression-related cognitive dysfunction model. After modeling, the DD + F group was treated with fluoxetine (10 mg/kg, ig) for 14 days. Behavioral tests were performed to assess changes in mood, cognition, learning, and social abilities. Histopathological observations were made to examine pathological changes, neuronal apoptosis, ultrastructure, and dendritic spine density in the prefrontal cortex. The concentration, relative expression level, and mRNA expression of VGLUT2 protein were also measured. Finally, a correlation analysis was performed between the relative expression level and mRNA expression of VGLUT2 protein and the pathological changes in neurons.Results: Compared to the CON group, the DD group exhibited decreased body weight, anhedonia, increased behavioral despair, reduced locomotor activity and spontaneous exploratory behavior, impaired spatial learning and memory, and decreased social interaction and social cognitive ability. Pathological damage was observed in the prefrontal cortex, with neuronal apoptosis, ultrastructural damage, and reduced neuroplasticity. The concentration, relative expression, and mRNA expression levels of VGLUT2 protein were decreased. Following fluoxetine intervention, the above behavioral phenotypes improved; pathological damage showed varying degrees of recovery; and the concentration, relative expression, and mRNA expression levels of VGLUT2 protein increased. Finally, there was a significant correlation between VGLUT2 protein expression and pathological changes in the prefrontal cortex.Conclusion: After 28 days of CUMS combined with isolation rearing, rats exhibited impairments in mood, cognition, learning, and social abilities, with neuronal damage and decreased VGLUT2 protein levels in the prefrontal cortex. Following fluoxetine intervention, VGLUT2 protein expression increased, neuronal repair in the prefrontal cortex occurred, depressive-like behavior improved, and cognitive learning and social abilities were restored.

Introduction: Non-suicidal self-injury (NSSI) is a prevalent concern among adolescents with depression, yet its relationship with demographic characteristics and physiological indicators remains underexplored. This study aimed to investigate these relationships among inpatient adolescents aged 13 to 18 at a hospital affiliated with Guizhou Medical University.Methods: A cross-sectional study was conducted involving 222 adolescent inpatients diagnosed with depression. Data on NSSI occurrence, demographic variables (gender, only-child status, age), and physiological indicators (ALT, TSH, FT4, PLR, TG, HDLC, LDLC, FT3, NLR, MLR) were collected and analyzed. Statistical analyses, including correlations and group comparisons, were performed to assess the associations between NSSI and these factors.Results: The prevalence of NSSI among the participants was 40.5%. Significant correlations were found between NSSI and several demographic and physiological factors. Specifically, NSSI was significantly associated with female gender, non-only-child status, younger age, lower ALT levels, higher TSH levels, lower FT4 levels, and higher PLR values. However, no significant differences were observed in TG, HDLC, LDLC, FT3, NLR, or MLR between the NSSI and non-NSSI groups.Discussion: The findings highlight distinct demographic and physiological profiles associated with NSSI among adolescents with depression. The prevalence rate of NSSI underscores its significance as a behavioral manifestation in this population. Further research should explore the underlying mechanisms linking these factors to better inform targeted interventions and treatment strategies for adolescents experiencing NSSI in the context of depression.

Purpose Major Depressive Disorder (MDD) and Insomnia Disorder (ID) are prevalent psychiatric conditions often occurring concurrently, leading to substantial impairment in daily functioning. Understanding the neurobiological underpinnings of these disorders and their comorbidity is crucial for developing effective interventions. This study aims to analyze changes in functional connectivity within attention networks and default mode networks in patients with depression and insomnia. Methods The functional connectivity alterations in individuals with MDD, ID, comorbid MDD and insomnia (iMDD), and healthy controls (HC) were assessed from a cohort of 174 participants. They underwent rs-fMRI scans, demographic assessments, and scale evaluations for depression and sleep quality. Functional connectivity analysis was conducted using region-of-interest (ROI) and whole-brain methods. Results The MDD and iMDD groups exhibited higher Hamilton Depression Scale (HAMD) scores compared to HC and ID groups (P < 0.001). Both ID and MDD groups displayed enhanced connectivity between the left and right orbital frontal cortex compared to HC (P < 0.05), while the iMDD group showed reduced connectivity compared to HC and ID groups (P < 0.05). In the left insula, reduced connectivity with the right medial superior frontal gyrus was observed across patient groups compared to HC (P < 0.05), with the iMDD group showing increased connectivity compared to MDD (P < 0.05). Moreover, alterations in functional connectivity between the left thalamus and left temporal pole were found in iMDD compared to HC and MDD (P < 0.05). Correlation analyses revealed associations between abnormal connectivity and symptom severity in MDD and ID groups. Conclusions Our findings demonstrate distinct patterns of altered functional connectivity in individuals with MDD, ID, and iMDD compared to healthy controls. These findings contribute to a better understanding of the pathophysiology of depression and insomnia, which could be used as a reference for the diagnosis and treatments of these patients.

Background: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) like liraglutide are primarily used for managing blood sugar levels in type 2 diabetes and aiding weight loss. Typically, their adverse effects are gastrointestinal, with limited exploration into their impact on mental health. Case presentation: This report examines a 39-year-old male with type 2 diabetes who developed depressive symptoms after starting liraglutide for glycemic control and weight reduction. Symptoms included poor mood, irritability, decreased interest and energy, progressing to sadness, low self-esteem, and physical discomfort. A clinical diagnosis of a depressive episode was made, coinciding with the initiation of liraglutide. Intervention and outcome: The patient depressive symptoms significantly improved within a week after discontinuing liraglutide and starting antidepressant therapy. This suggests a possible link between liraglutide and depression, despite considering other factors like diabetes-related stress. Discussion: The report explores potential mechanisms, such as GLP-1RA effects on glucose fluctuations and dopamine modulation, which might contribute to depressive symptoms. The influence on the brain reward system and the reduction in cravings for addictive substances after GLP-1RA use is also discussed as a factor in mood regulation. Conclusion: This case highlights the necessity of being vigilant about potential psychiatric side effects, particularly depression, associated with GLP-1RAs. The rarity of such reports calls for more research to investigate and understand these implications further.

Background: Non-suicidal self-injury (NSSI), of which the predisposing factors are complex and diverse, profoundly affects the physical and mental health of young people. Therefore, this work established an NSSI intermediary network model considering the interaction of multiple factors. A mediating effect between attention-deficit/hyperactivity disorder (ADHD) and NSSI, considering the influence of comorbidities, such as depression, anxiety, and impulsive personality, was proposed based on sex differences. Methods: A total of 2,689 middle school students in Ningbo City, Zhejiang Province, China, were randomly sampled and participated in this study. Data regarding their demographic characteristics, attention deficit, hyperactivity/impulsivity, NSSI, anxiety, depression, internet addiction, and other comorbid symptoms were collected and analyzed. After initially screening the data, variables were assessed for significance using a single-factor inter-group difference analytic method, and a binary logistic regression analysis was performed. The intermediary effect of factors influencing NSSI in males and females was also analyzed. Results: The overall NSSI rate was 15.16%. The results showed that the impact of individual impulsivity characteristics (impulsiveness, the ADHD with hyperactivity/impulsivity subtype) on NSSI behavior was not significant (regression results, P > 0.05). The degree of association between ADHD with attention deficit and ADHD with comprehension deficit subtypes, and other comorbid symptoms (depression, anxiety, and internet addiction disorder) and NSSI, with odds ratios (ORs) of 7.6/6.42/436.68/3.82/1.86, and 95% bootstrap confidence intervals (CIs) of 4.64, 12.87/3.46, 12.67/137.42, 2659.13/2.32, 6.37/1.31, 2.82, respectively. The results also showed significant effects of ADHD subtypes on comorbid symptoms and the path effects of NSSI (P < 0.01). Among them, the mediating effect was the strongest when anxiety was the mediating variable, and the mediating effect of girls was higher than that of boys. Conclusion: The results of this work demonstrated the influence of ADHD symptoms on NSSI behavior. Among patients with ADHD, patients with subtypes with obvious attention deficit characteristics were more likely to exhibit NSSI behavior, whereas the hyperactive impulse subtype had no direct impact on NSSI. We conclude that adolescent impulsivity may not be directly related to NSSI behavior and that impulsive characteristics jointly affect NSSI behavior through a series of NSSI comorbid symptoms. Notably, the probability of symptom onset and the degree of comorbidity was significantly higher in girls than in boys of the same age, and girls were more prone to NSSI behavior. These findings provide effective theoretical support for the prevention and treatment of adolescent NSSI behavior.

Objective. This paper aimed to probe changes in the default mode network (DMN) functional connectivity (DMNFC) of the brain of patients with insomnia disorder (ID) under the resting state. Methods. A total of 67 patients with ID and 67 graphically matched healthy controls were selected. Then, their general information was collected, followed by a psychological scale valuation. Resting state functional magnetic resonance imaging (rs‐fMRI) scanning was conducted. Subsequently, collected statistics were processed, bilateral precuneus and medial superior frontal gyrus were defined as regions of interest (ROI), and the difference in intensity between these two groups was compared. Results. Compared with the healthy control group, the patients in the ID group were observed with abnormalities of DMNFC. Specifically, a significant increase in the functional connectivity (FC) could be observed between the left medial superior frontal gyrus and left central anterior gyrus, the left medial superior frontal gyrus and anterior cingulate gyrus, the right medial superior frontal gyrus and left central anterior gyrus, the left anterior cuneiform and left central anterior/posterior gyrus, the left anterior cuneiform and left superior occipital gyrus, as well as the right anterior cuneiform and left central posterior gyrus. However, the FC between the left anterior cuneiform and the right middle frontal gyrus was weakened, as well as between the left anterior cuneiform and the right angle gyrus and between the right precuneus and the left inferior temporal gyrus. Conclusion. ID patients may suffer changes in FC. The decline of FC in DMN may be one of the underlying causes of ID; the enhancement of FC between DMN and the visual‐spatial attention network may play a key role in the mechanisms of impaired brain functional networks of ID.