Major depressive disorder (MDD) is a common and complex mental disorder, that adversely impacts an individual’s quality of life, but its diagnosis and treatment are not accurately executed and a symptom-based approach is utilized in most cases, due to the lack of precise knowledge regarding the pathophysiology. So far, the first-line treatments are still based on monoamine neurotransmitters. Even though there is a lot of progress in this field, the mechanisms seem to get more and more confusing, and the treatment is also getting more and more controversial. In this study, we try to review the broad advances of monoamine neurotransmitters in the field of MDD, and update its effects in many advanced neuroscience studies. We still propose the monoamine hypothesis but paid special attention to their effects on the new pathways for MDD, such as inflammation, oxidative stress, neurotrophins, and neurogenesis, especially in the glial cells, which have recently been found to play an important role in many neurodegenerative disorders, including MDD. In addition, we will extend the monoamine hypothesis to basic emotions; as suggested in our previous reports, the three monoamine neurotransmitters play different roles in emotions: dopamine—joy, norepinephrine—fear (anger), serotonins—disgust (sadness). Above all, this paper tries to give a full picture of the relationship between the MDD and the monoamine neurotransmitters such as DA, NE, and 5-HT, as well as their contributions to the Three Primary Color Model of Basic Emotions (joy, fear, and disgust). This is done by explaining the contribution of the monoamine from many sides for MDD, such the digestive tract, astrocytes, microglial, and others, and very briefly addressing the potential of monoamine neurotransmitters as a therapeutic approach for MDD patients and also the reasons for its limited clinical efficacy, side effects, and delayed onset of action. We hope this review might offer new pharmacological management of MDD.

Purpose: The aim of this study was to investigate the relationship between stressful life events and sleep quality and to probe the role of rumination and resilience in the relationship. Method: The Adolescent Self-Rating Life Events Checklist, Ruminative Responses Scale, Connor–Davidson Resilience Scale, and Pittsburgh Sleep Quality Index were used among 1,065 college students. Statistical Product and Service Solutions (SPSS) 20.0 and the SPSS macro Process, which were specifically developed for assessing complex models including both mediators and moderators, were used to analyze the data. Results: High scores of stressful life events predicted worse sleep quality. Rumination partially mediated the relations between stressful life events and sleep quality. Resilience moderated the direct and indirect paths leading from stressful life events to sleep quality. Conclusions: The results demonstrate that stressful life events can directly affect the sleep quality of college students and indirectly through rumination. Additionally, increasing psychological resilience could decrease both the direct effect and the indirect effect of stressful life events affecting sleep quality. The results of this study may contribute to a better understanding of the effects, as well as the paths and conditions, of stressful life events on sleep quality in college students. Moreover, these findings can provide constructive suggestions for improving college students’ sleep quality.

Major Depression disorder (MDD) is a potentially life-threatening mental illness, however, many patients have a poor response to current treatments. Recent studies have suggested that stress- or trauma-induced oxidative stress and inflammation could be important factors involved in the development of MDD, but the mechanisms remain unclear. We showed that the glymphatic system is a recently discovered structure in the brain that may be involved in the clearance of large molecular and cell debris in extracellular space. In addition, the glymphatic system can help with the removal of reactive oxygen species (ROS) and cytokines such as IL-1β and HIF-1α. Glymphatic impairment can lead to ROS accumulation in the microenvironment, inducing cellular injury signaling and activating NLRP3 in microglia to induce inflammation and, thus, many brain diseases, including psychiatric disorders. Therefore, trauma-induced glymphatic impairment could induce oxidative stress and inflammation, and thus MDD. This paper will review recent advances with regard to stress-induced glymphatic system impairment and ROS-mediated inflammation in MDD.

Objective: Recently, many emotional diseases, such as anxiety and depression, have prevailed, and it is expected that emotional disease will be the leading cause of social and economic burden in 2030. These emotional diseases may be due to certain personality traits, which could be the reasons for the development of mental illness. Personality theories have been constantly developed over the past hundreds of years, and different dimensions of personality traits corresponding to different physiological bases and emotional feelings have been proposed. However, personality may be the least studied area in psychology. Methods: In this paper, we will give a short review on the development of personality theories as well as dimensional emotional theory. Then, we will compare the similarities between the emotional dimension and personality dimension. Furthermore, we will also investigate the neural mechanisms of personality and emotions, focusing on neuromodulators for anxiety-related personality traits, in order to provide a clear relationship between different neurotransmitters and anxiety-related personality traits. Results: The results of our study suggest that the emotional dimension and personality dimension may be somewhat related, for example, the extrovert/introvert dimension of personality might be related to the hedonic dimension, which includes happiness/sadness, and the neurotic dimensions might be related to emotional arousal. In addition, our study found that personality traits are also related to basic emotions, for instance, people who are too self-centered are prone to feeling a mood of disgust or depression, while anger and fear correspond to unstable personality traits. The analysis suggested that the neural substrates of both personality and emotions might be described as follows: extroverted–joy–dopamine (DA); introverted–disgust–5-hydroxytryptamine (5-HT); unstable (neuroticism)–anger/fear–noradrenaline (NE); stable–calmness. Conclusions: The results of this study suggest that there is a correlation between personality traits and emotions, and both depend on monoamine neurotransmitters (dopamine, norepinephrine and serotonin). In addition, personality disorders can be interfered via the regulation of emotions and neurotransmitters. This paper opens up a whole new perspective for future research on personality traits and emotional diseases and has great clinical value and practical significance.

With an increase in the number of international students in China, there has been a simultaneous increase in their emotional problems, such as depression, as well as the importance of their emotional well-being. This study aimed to investigate the influence of social support on depression and the mediation and moderation mechanisms of this relationship in international students. In total, 349 international students in China responded to a questionnaire survey comprising the Social Support Rating Scale, Self-rating Depression Scale, Adult Attachment Scale, and Self-Esteem Scale. The results showed that: (1) attachment closeness had a significant direct predictive effect on depression; (2) attachment closeness played a mediating role in the relationship between social support and depression; and (3) the direct effect of social support on depression and the mediating effect of attachment and closeness are regulated by self-esteem. Therefore, interventions aimed at improving the social support, attachment closeness, and self-esteem of international students in China can be effective in reducing their depressive symptoms.

With the development of social economics and the increase of working pressure, more and more women are suffering from long-term serious stress and showing symptoms of perimenopausal depression (PMD). The incidence rate of PMD is increasing, and the physical and mental health are seriously affected. However, due to the lack of accurate knowledge of pathophysiology, its diagnosis and treatment cannot be accurately executed. By consulting the relevant literature in recent years, this paper elaborates the neuroendocrine mechanism of perimenopausal depression from the aspects of epigenetic changes, monoamine neurotransmitter and receptor hypothesis, glial cell-induced neuroinflammation, estrogen receptor, interaction between HPA axis and HPG axis, and micro-organism-brain gut axis. The purpose is to probe into new ways of treatment of PMD by providing new knowledge about the neuroendocrine mechanism and treatment of PMD.