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Background: Chronic ethanol exposure (CEE) is recognized as an important risk factor for depression, and the gut-brain axis has emerged as a key mechanism underlying chronic ethanol exposure-induced anxiety and depression-like behaviors. Short-chain fatty acids (SCFAs), which are the key metabolites generated by gut microbiota from insoluble dietary fiber, exert protective roles on the central nervous system, including the reduction of neuroinflammation. However, the link between gut microbial disturbances caused by chronic ethanol exposure, production of SCFAs, and anxiety and depression-like behaviors remains unclear., Methods: Initially, a 90-day chronic ethanol exposure model was established, followed by fecal microbiota transplantation model, which was supplemented with SCFAs via gavage. Anxiety and depression-like behaviors were determined by open field test, forced swim test, and elevated plus-maze. Serum and intestinal SCFAs levels were quantified using GC-MS. Changes in related indicators, including the intestinal barrier, intestinal inflammation, neuroinflammation, neurotrophy, and nerve damage, were detected using Western blotting, immunofluorescence, and Nissl staining., Results: Chronic ethanol exposure disrupted with gut microbial homeostasis, reduced the production of SCFAs, and led to anxiety and depression-like behaviors. Recipient mice transplanted with fecal microbiota that had been affected by chronic ethanol exposure exhibited impaired intestinal structure and function, low levels of SCFAs, intestinal inflammation, activation of neuroinflammation, a compromised blood-brain barrier, neurotrophic defects, alterations in the GABA system, anxiety and depression-like behaviors. Notably, the negative effects observed in these recipient mice were significantly alleviated through the supplementation of SCFAs., Conclusion: SCFAs not only mitigate damage to intestinal structure and function but also alleviate various lesions in the central nervous system, such as neuroinflammation, and reduce anxiety and depression-like behaviors, which were triggered by transplantation with fecal microbiota that had been affected by chronic ethanol exposure, adding more support that SCFAs serve as a bridge between the gut and the brain., (© 2024. The Author(s).)

Emerging adulthood is a pivotal period for romantic relationships, yet the specific mechanisms through which attachment anxiety influences relationship dynamics and psychological outcomes in this phase are poorly understood. Particularly, in the context of romantic dyads, understanding how partners' behaviors and emotional patterns reciprocally influence each other remains underexplored. This study utilizes the Actor-Partner Interdependence Model and Actor-Partner Interdependence Mediator Model to explore the relationship between attachment anxiety,relational aggression (both perpetration and victimization), and depressive symptoms among emerging adults. A sample of 138 mixed-sex emerging adulthood couples from China, was recruited (M age  = 21.40, SD = 2.54; 50% female, 62.6% reporting that this relationship was ongoing for more than a year). Attachment anxiety significantly predicted relational aggression in both partners, with male attachment anxiety also significantly predicted female relational aggression. Significant indirect effects of both partners' relational aggression perpetration and victimization on their own and each other's relationship between attachment anxiety and depressive symptoms. These findings contribute to understanding the intricate dynamics of attachment anxiety and relational aggression in romantic relationships during emerging adulthood, emphasizing the need for targeted interventions to mitigate these risks., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Negative emotions and gut microbiota during pregnancy both bear significant public health implications. However, the relationship between them has not been fully elucidated. This study, utilizing data from a pregnancy cohort, employed metagenomic sequencing to elucidate the relationship between anxiety, depression, and gut microbiota's diversity, composition, species, and functional pathways. Data from 87 subjects, spanning 225 time points across early, mid, and late pregnancy, were analyzed. The results revealed that anxiety and depression significantly corresponded to lower alpha diversity (including the Shannon entropy and the Simpson index). Anxiety and depression scores, along with categorical distinctions of anxiety/non-anxiety and depression/non-depression, were found to account for 0.723%, 0.731%, 0.651%, and 0.810% of the variance in gut-microbiota composition ( p = 0.001), respectively. Increased anxiety was significantly positively associated with the abundance of Oscillibacter sp. KLE 1745 , Oscillibacter sp. PEA192 , Oscillibacter sp. KLE 1728 , Oscillospiraceae bacterium VE202 24 , and Treponema socranskii . A similar association was significantly noted for Oscillibacter sp. KLE 1745 with elevated depression scores. While EC.3.5.3.1: arginase appeared to be higher in the anxious group than in the non-anxious group, vitamin B12-related enzymes appeared to be lower in the depression group than in the non-depression group. The changes were found to be not statistically significant after post-multiple comparison adjustment.

The microbiota-gut-brain axis is a bidirectional regulatory pathway between the brain and the gastrointestinal tract, which plays an important role in maintain homeostasis. Gut microbiota could influence the behavior, cognition, stress response and others via the axis. Depression is a complex psychiatric disease, giving rise to heavy social health and economic burden. In recent years, studies have shown that the gut microbiota are closely linked to the pathophysiological processes of depression. In this article, the interaction and its underlying mechanisms between depression and gut microbiota were summarized., Competing Interests: Declaration of Competing Interest All authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The current study aims to track the changes in the levels of smart phone addiction (SPA) and depressive symptoms between pre and during COVID-19 and potential risk factors of among Chinese college students in a four-wave longitudinal study., Methods: The participants were recruited from a Chinese university (n = 195; 58.5% females). The first three-wave surveys were conducted before COVID-19 (during December of Year 1, June of Year 1, and December of Year 2 of their college study; Time 1, Time 2, Time 3), while the fourth survey (Time 4; during June of Year 2 of their college study) was conducted in June 2020 during COVID-19. COVID-19-related factors, including quarantine, lockdown, boredom, emotional loneliness, and social loneliness, were investigated., Results: The results showed a significant increase in the levels of depressive symptoms and prevalence of probable depression during COVID-19 (69.2%) compared to those 18 months, 12 months and 6 months before COVID-19 (41.5, 45.6, 48.2%) but non-significant changes in SPA. Boredom and emotional loneliness were positively associated with both SPA and depressive symptoms during COVID-19. Social loneliness was also positively associated with depressive symptoms during COVID-19. Quarantine and lockdown were not significantly associated with SPA or depressive symptoms., Discussion and Conclusions: The results highlight that the study population may be a high risk group of probable depression. Future studies should continue to track these mental and behavioral status with the progression of the epidemic. The identified emotional factors could be used to reduce depressive symptoms during COVID-19 and prevent the potential risk of SPA.

Quarantine plays a key role in controlling the pandemic of 2019 coronavirus disease (COVID-19). This study investigated (a) the associations between mandatory quarantine status and negative cognitions (perceived discrimination because of COVID-19 and perceived risk of COVID-19 infection)/mental health status (emotional distress because of COVID-19, probable depression, and self-harm/suicidal ideation), (b) the associations between the negative cognitions and mental health status, and (c) potential mediations between quarantined status and probable depression and self-harm/suicidal ideation via COVID-19-related negative cognitions/emotional distress. An online cross-sectional survey was conducted among 24,378 students of 26 universities in 16 Chinese cities (February 1-10, 2020). Correlation coefficients, odds ratios (OR), structural equation modeling, and other statistics were used for data analysis. Mandatory quarantined status was significantly and positively associated with perceived discrimination (Cohen's d = 0.62), perceived high/very high risk of infection (OR = 1.61), emotional distress (Cohen's d = 0.46), probable depression (OR = 2.54), and self-harm/suicidal ideation (OR = 4.98). Perceived discrimination was moderately and positively associated with emotional distress (Spearman correlation = 0.44). Associations between perceived risk of infection and mental health variables were significant but relatively weak. Cross-sectional mediation models showed good model fit, but the overall indirect paths via COVID-19-related negative cognitions/emotional distress only accounted for 12-15% of the total effects between quarantined status and probable depression and self-harm/suicidal ideation. In conclusion, quarantined participants were more likely than others to perceive discrimination and exhibit mental distress. It is important to integrate mental health care into the planning and implementation of quarantine measures. Future longitudinal studies to explore mechanisms underlying the mental health impact of quarantines are warranted. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Background: During an epidemic, both frontline and non-frontline medical staff endure stressful work circumstances that render their mental health a major public health concern. This study aims at investigating and comparing the prevalence and severity of mental health symptoms (i.e., anxiety, depression and insomnia) between frontline medical staff and non-frontline medical staff during the coronavirus disease 2019 (COVID-19) outbreak. It also seeks to evaluate the association of their mental health with occupational stress. Methods: A cross-sectional study was conducted in Wenzhou, China from 2020 February 16th to 2020 March 2th. A total of 524 medical staff responded to the Generalized Anxiety Disorder Scale, the Patient Health Questionnaire, the Insomnia Severity Index, the Occupational stress Questionnaire, and a demographic data form. Data were principally analyzed with logistic regression. Results: Of the 524 participants, 31.3% reported depression, 41.2% reported anxiety, and 39.3% reported insomnia. Compared with the citizens during the COVID-19 epidemic, medical staff experienced higher level of anxiety, depression and insomnia, especially the frontline medical staff. Furthermore, male, married medical staff with poorer physical health reported lower mental health. Frontline medical staff endorsed higher self-reported occupational stress, especially higher occupational hazards, than non-frontline medical staff. In addition, four indicators on occupational stress (working intensity, working time, working difficulty and working risk) were correlated positively with mental health symptoms. Regression analyses found a significant association between occupational stress and mental health symptoms in both frontline and non-frontline medical staff during COVID-19 outbreak. Conclusion: The results indicated that during the COVID-19 epidemic, medical staff experienced higher levels of anxiety, depression and insomnia than citizens, and their occupational stress had positive effects on their psychological distress. These findings emphasize the importance of occupational stress management interventions to decrease the risk of developing mental health problems among the medical staff during a biological disaster. [ABSTRACT FROM AUTHOR]

Background: This 3-year longitudinal study investigated the prospective relationships between mobile phone dependence and mental health status (i.e., subjective well-being, anxiety and depression) and the mediating role of college adjustment among Chinese undergraduate students.Methods: The study recruited 265 first-year undergraduate students from a university (mean age = 18.95 years, SD = 0.72) in Wenzhou, China. A baseline survey and two follow-up surveys were conducted between November 2013 and December 2015 (the response rate was 76.4%). The validated Mobile Phone Addiction Tendency Scale (MPATS), Chinese College Student Adjustment Scale (CCSAS), Index of Well-being, Self-rating Anxiety Scale (SAS), and Self-rating Depression Scale (SDS) were used for assessments.Results: The prevalence of anxiety and depression at Year 3 was 7.5% and 9.4%, respectively. Correlation analyses showed that mobile phone dependence at Year 1, college adjustment at Year 2, and mental health status at Year 3 were significantly correlated with each other. Structural equation modeling analyses showed that mobile phone dependence at Year 1 significantly predicted poor mental health status at Year 3. College adjustment at Year 2 significantly mediated the effect of mobile phone dependence at Year 1 on mental health status at Year 3.Conclusions: Interventions both on reduction of mobile phone dependency and improvement of college adjustment (especially among those with mobile phone dependence) are possible and needed among new college students to prevent their future depression and anxiety. Such interventions should be incorporated into regular education programs in universities. [ABSTRACT FROM AUTHOR]

Tau protein is known to play an important role in maintaining microtubule assembly and stabilization, and maintaining the normal morphology of neurons, but several studies have found that chronic stress leads to Tau hyperphosphorylation. A large number of clinical trials have found that ketamine, which is an N-methyl-D-aspartate receptor antagonist, produces a rapid, long-lasting, and potent antidepressant effect in patients suffering from major depression. This rapid antidepressant effect of ketamine, which involves many mechanisms, has attracted wide attention. However, the relationship between ketamine's antidepressant effects and Tau protein has rarely been examined. We used C57BL/6 and Tau KO mice exposed to 42 days of chronic unpredictable mild stress (the CUMS model) to investigate the effect of ketamine on behavioral changes and synaptic functioning of the hippocampus. The results showed that a single treatment of ketamine rapidly relieved the CUMS-induced anhedonia, depression-like, and anxious behaviors of the C57BL/6 mice. The abnormal behaviors were accompanied by increased levels of specific alterations of hyperphosphorylated Tau protein in cytoplasm and synapse in the hippocampus of the C57BL/6 mice, but ketamine reduced the aggregation of hyperphosphorylated Tau protein only in the synapse. We also found that CUMS exposure reduced the levels of GluA1 and PSD95 in the hippocampus of the C57BL/6 mice and that these deficits were reversed by ketamine. However, the Tau KO mice did not develop any stress-induced depressive behaviors or deficits of hippocampal function. The antidepressant effect of ketamine may decrease the levels of hyperphosphorylated Tau protein in synapse of C57BL/6 mice. [ABSTRACT FROM AUTHOR]

Background: The COVID-19 epidemic may elevate mental distress and depressive symptoms in various populations in China. Objective: This study investigates the levels of depression and mental distress due to COVID-19, and the associations between cognitive, behavioral, and psychosocial factors, and depression and mental distress due to COVID-19 among university students in China. Methods: A large-scale online cross-sectional study (16 cities in 13 provinces) was conducted among university students from February 1 to 10, 2020, in China; 23,863 valid questionnaires were returned. The Patient Health Questionnaire-9 was used to assess depression. Structural equation modeling was performed to test mediation and suppression effects. Results: Of the 23,863 participants, 47.1% (n=11,235) reported high or very high levels of one or more types of mental distress due to COVID-19; 39.1% (n=9326) showed mild to severe depression. Mental distress due to COVID-19 was positively associated with depression. All but one factor (perceived infection risks, perceived chance of controlling the epidemic, staying at home, contacted people from Wuhan, and perceived discrimination) were significantly associated with mental distress due to COVID-19 and depression. Mental distress due to COVID-19 partially mediated and suppressed the associations between some of the studied factors and depression (effect size of 6.0%-79.5%). Conclusions: Both mental distress due to COVID-19 and depression were prevalent among university students in China; the former may have increased the prevalence of the latter. The studied cognitive, behavioral, and psychosocial factors related to COVID-19 may directly or indirectly (via mental distress due to COVID-19) affect depression. Interventions to modify such factors may reduce mental distress and depressive symptoms during the COVID-19 epidemic. JMIR Ment Health 2021;8(2):e22705 doi:10.2196/22705 [ABSTRACT FROM AUTHOR]

Chronic ethanol exposure (CEE) is associated with greater neurodegenerative effects and an increased risk of depression disorder. The AMPAR is thought to be involved in depression and a reduction in its GluA1 subunit was observed in the mouse hippocampus after CEE. AMPAkines are positive allosteric modulators of the AMPA receptor and have improved depressive-like behavior. However, the role of AMPARs in CEE-induced depressive-like behavior is not clear. It is unclear whether AMPAkines, positive allosteric agonists of AMPARs, protect against ethanol-induced depression. We investigated the effects of CX516 on ethanol-induced depressive-like behavior in a mouse model. CX516 (5 mg/kg) administration alleviated 20% (m/V) ethanol-induced depressive-like behavior in mice. Furthermore, CX516 significantly diminished the inhibition of the ERK1/2-BDNF-TrkB pathway in the hippocampus of ethanol-exposed mice. In addition, CX516 attenuated the levels of pro-inflammatory (IL-6, IL-1β), apoptosis (BAX, BCL-2), and neurodegeneration (FJC) in the mouse hippocampus induced by CEE. [Display omitted] • CX516 alleviated chronic ethanol exposure (CEE)-induced depressive-like behavior. • CX516 attenuated CEE-induced hippocampal neurodegeneration. • CX516 attenuated CEE-induced apoptosis and inflammation in hippocampus. • CX516 had limited effects on the expression of synaptic proteins. [ABSTRACT FROM AUTHOR]

• Chronic ethanol exposure caused depressive-like behavior in mice. • GluA1 in the mouse hippocampus was downregulated by chronic ethanol exposure. • Chronic ethanol exposure caused depression-associated changes in the mouse hippocampus. • Ethanol-induced depression-associated changes were aggravated by GluA1. Chronic ethanol exposure can increase the risk of depression. The α-amino-3‑hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor is a key factor in depression and its treatment. The study was conducted to investigate the depressive-like behavior induced by chronic ethanol exposure in mice and to explore the mechanism in cells. To establish the chronic ethanol exposure mouse model, male C57BL/6 N mice were administered 10% (m/V) and 20% (m/V) ethanol as the only choice for drinking for 60 days, 90 days and 180 days. Depressive-like behavior in mice was confirmed by the forced swimming test (FST). Ethanol-induced changes in the mouse hippocampus were indicated by Western blotting, qPCR and Fluoro-Jade C (FJC) staining. We confirmed that 90- and 180-day ethanol exposure can lead to depressive-like mouse behavior, cell apoptosis, neuronal degeneration, a reduction in GluA1 and brain-derived neurotrophic factor (BDNF) expression, and an increase in IL-6 and IL-1β in the mouse hippocampus. GluA1 silencing and overexpression models of SH-SY5Y cells were established for further investigation. The cells were treated with 100 mM and 200 mM ethanol for 24 h. Ethanol exposure decreased cell viability and the expression of BDNF and increased the cell apoptosis rate and the expression of BAX, cleaved caspase-3, IL-1β and IL-6. GluA1 silencing aggravated ethanol-induced changes in cell viability and apoptosis and the expression of BDNF, BAX and cleaved caspase-3, and GluA1 overexpression attenuated these changes. Neither the silencing nor overexpression of GluA1 had an effect on ethanol-induced increases in IL-1β and IL-6. Our results indicated that chronic ethanol exposure induced depressive-like behavior in male C57BL/6 N mice by downregulating GluA1 expression. [ABSTRACT FROM AUTHOR]

Recent research shows that problematic smartphone use is a risk factor for individual depression, however, little is known about the mediating and moderating mechanisms underlying this relation. The present study investigated (a) the mediating role of procrastination in the association between problematic smartphone use and adolescent depression, and (b) the moderating role of perceived social support in the relationships between problematic smartphone use and adolescent depression. This model was examined with 772 Chinese adolescents (mean age = 16.81 years, SD = 0.73). The results indicated that problematic smartphone use was positively related to adolescent depression. Mediation analyses revealed that procrastination partially mediated this relationship. Moderated mediation further indicated perceived social support moderated the link between procrastination and adolescent depression, with the effect being significant only for adolescents with a low level of perceived social support. These findings highlight the importance of identifying the mechanisms that moderate the mediated paths between problematic smartphone use and adolescent depression. • Problematic smartphone use (PSU) is related to depression (Dep). • Procrastination (Pro) mediates the link between PSU and Dep. • Perceived social support moderates the link between Pro and Dep. [ABSTRACT FROM AUTHOR]