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.

Sleep constitutes an essential physiological process that is vital for maintaining physical and mental wellbeing. However, the science of sleep focusing on basic questions such as “how” we sleep and “why” we sleep is still not clear. Over the past decade, substantial progress has also been made in elucidating the interactions between sleep and other biological processes, providing insights into the basic questions of sleep. Among these, emerging evidence highlights the microbiota-gut-brain axis (MGBA) as a pivotal bidirectional network that connects gut microorganisms with the central nervous system to regulate sleep architecture and homeostasis. This interaction is inherently bidirectional: sleep deprivation alters gut motility, mucosal integrity, and microbial composition, while microbial metabolites in turn influence neurotransmission ( γ -aminobutyric acid, serotonin), immune-endocrine balance, and inflammatory signaling. In this article, we will review recent studies about MGBA-targeted therapeutic strategies for sleep disorders, such as probiotics, prebiotics, and fecal microbiota transplantation, which aim to restore microbial homeostasis and improve sleep quality. Furthermore, we discuss emerging interventions that modulate microbial metabolites and neuroimmune-endocrine signaling, as well as innovative pharmacological approaches targeting MGBA dysfunction. Collectively, we hope this review will contribute to a deeper understanding of MGBA-mediated mechanisms in sleep disorders promises to inform novel preventive and therapeutic strategies, ultimately improving clinical outcomes and quality of life for affected individuals.

Objective: Major depressive disorder (MDD) is one of the most common psychiatric disorders, the diagnosis and treatment of MDD are major clinical issues. However, there is a lack of effective biomarkers and drugs diagnosis and therapeutics of MDD. In the present study, bioinformatics analysis combined with an experimental verification strategy was used to identify biomarkers and paeoniflorin targets for MDD diagnosis and treatment.Methods: Based on network pharmacology, we obtained potential targets and pathways of paeoniflorin as an antidepressant through multiple databases. We then constructed a protein-protein interaction network and performed enrichment analyses. According to the results, we performed in vivo and in vitro experimental validation.Results: The results showed that paeoniflorin may exert an antidepressant effect by regulating cell inflammation, synaptic function, NF-κB signaling pathway, and intestinal inflammation.Conclusion: NPM1, HSPA8, HSPA5, HNRNPU, and TNF are the targets of paeoniflorin treatment. In addition, we demonstrated that paeoniflorin inhibits inflammatory cytokine production via the p38MAPK/NF-κB pathway and has neuroprotective effects on the synaptic structure. Our findings provide valuable evidence for the diagnosis and treatment of MDD.

Background: Major depressive disorder (MDD), characterised by persistent anhedonia and elevated suicide risk, represents a global mental health challenge. Recent studies suggest a link between gut–brain axis dysfunction and depression. The natural compound paeoniflorin demonstrates clinically relevant antidepressant effects, yet its underlying neurobiological mechanisms remain elusive. Aims: This study aims to examine how paeoniflorin alleviates depression‐like behaviours in rats subjected to chronic unpredictable mild stress (CUMS) by modulating the function of gut–brain axis, and explore the connections between gut microbiota, metabolites and MDD. Methods: Depression‐like behaviours in rats were induced by CUMS, and the antidepressant effect of paeoniflorin was assessed using behavioural tests. The composition and function of the intestinal microbiota were analysed using 16S rRNA sequencing, and metabolomic analysis was performed on serum, hippocampus, jejunum and faecal samples. Enzyme‐linked immunosorbent assay and hematoxylin and eosin staining were used to detect the levels of inflammatory factors and cortisol, as well as the infiltration of inflammatory cells in the jejunum of rats after cohousing. Long‐term potentiation assays and Golgi staining were used to detect dendritic spine density and synaptic plasticity, respectively. Results: Paeoniflorin significantly alleviated depression‐like behaviours and cognitive deficits in CUMS rats. 16S rRNA sequencing revealed that paeoniflorin improved the abundance and diversity of the gut microbiota in CUMS rats. Enrichment of differential metabolites in the brain, intestine, faeces and serum revealed a primary accumulation in the amino acid metabolism pathway. We further observed a correlation between the relative abundance of microbial communities and metabolites. Cohousing experiments verified that microbial metabolites of paeoniflorin can reduce neuroinflammation and improve synaptic plasticity. Conclusions: Disruptions in gut microbiota and its metabolites impair gut–brain interactions. Paeoniflorin's neuroprotective and antidepressant effects are mediated through the modulation of the function of the gut–brain axis.

Major depressive disorder is a severe mental health condition characterized by persistent depressed mood and loss of interest. Current first-line pharmacotherapies often exhibit limited therapeutic performance and adverse side effects. Transcutaneous auricular vagus nerve stimulation (taVNS) is a promising, safe, and noninvasive alternative intervention with demonstrated neuromodulatory efficacy. Nevertheless, its mechanisms remain unclear. This study investigated whether the antidepressant properties of taVNS are associated with the microbiota-gut-brain axis, focusing on the potential crosstalk between differentially expressed hippocampal proteins and the gut microbiota. A chronic unpredictable mild stress (CUMS) rat model of depression was established, and taVNS was administered for 14 days. Hippocampal proteomic profiling was performed using data-independent acquisition. Fecal metagenomic sequencing was conducted to characterize alterations in gut microbial communities. Key signaling pathways were validated using Western blot, qRT-PCR, HE staining, and transmission electron microscopy, all of which were employed to systematically assess behavioral, proteomic, microbial, and molecular changes. Proteomics and molecular analyses revealed that taVNS upregulated hippocampal expression of glutamate ionotropic receptor N-methyl-D-aspartate type subunit 1 (GluN1) and brain-derived neurotrophic factor (BDNF), while simultaneously restoring mitogen-activated protein kinase (MAPK) signaling activity. Metagenomic profiling demonstrated that taVNS increased the abundance of Akkermansia muciniphila and reduced Ligilactobacillus reuteri. Ligilactobacillus levels were positively correlated with synaptogyrin-1 (Syngr1), indicating their potential association in enhancing the antidepressant effects mediated by the GluN1/MAPK/BDNF signaling cascade. TaVNS significantly alleviated depression-like behaviors in CUMS-exposed rats. The underlying mechanism may involve the restoration of synaptic function of glutamatergic neurons by regulating the GluN1/MAPK/BDNF signaling pathway. In addition, taVNS reshaped the gut microbiota, markedly increasing the abundance of Akkermansia muciniphila and Ligilactobacillus murinus while reducing Limosilactobacillus reuteri and Lactobacillus johnsonii. The positive correlation between Syngr1 protein level and Ligilactobacillus abundance in the hippocampus suggests that the microbiota-gut-brain axis may play a key role in the antidepressant effects of taVNS.

Major depressive disorder (MDD) is associated with immune dysregulation, but the contribution of chemotaxis-related genes remains incompletely understood. This study aimed to identify chemotaxis-related signatures in MDD and evaluate their diagnostic relevance. Two peripheral-blood microarray datasets (GSE76826 and GSE38206) were integrated after batch correction, and differentially expressed genes were intersected with the GOBP_TAXIS gene set. Hub genes were selected using random forest and SVM-RFE and evaluated by logistic regression, ROC, calibration, and decision curve analyses. Immune-cell abundance, molecular subtypes, single-nucleus expression, and in silico gene-knockout effects were further examined, followed by qRT-PCR and Western blot validation in a CUMS rat model. The integrated cohort included 21 controls and 29 MDD cases. GOBP_TAXIS activity was increased in MDD (p < 0.001), and seven candidate genes yielded three upregulated hub genes (CXCL2, NRG1, and C3AR1). The fixed three-gene model yielded an exploratory AUC of 0.889 in the development cohort. All three genes correlated positively with monocytes/neutrophils and negatively with T cells. Single-cell analysis revealed cell-specific enrichment, while in silico knockout simulations predicted transcriptional changes involving RORB and NTNG1 following virtual perturbation of CXCL2 and NRG1. Animal experiments confirmed consistent upregulation at both transcriptional and translational levels. CXCL2, NRG1, and C3AR1 represent candidate chemotaxis-related biomarkers for MDD and are associated with distinct immune-cell abundance patterns and inflammatory signatures, warranting further functional validation.