The microbiota–gut–brain (MGB) axis is a complex communication network linking the gut, microbiota, and brain, influencing various aspects of health and disease. Dysbiosis, a disturbance in the gut microbiome equilibrium, can significantly impact the MGB axis, leading to alterations in microbial composition and function. Emerging evidence highlights the connection between microbiota alterations and neurological and psychiatric disorders, including depression. This review explores the potential of psychobiotics in managing depressive disorders, emphasizing their role in restoring microbial balance and influencing the MGB axis. Psychobiotics exhibit positive effects on the intestinal barrier, immune response, cortisol levels, and the hypothalamic–pituitary–adrenal (HPA) axis. Studies suggest that probiotics may serve as an adjunct therapy for depression, especially in treatment-resistant cases. This review discusses key findings from studies on psychobiotics interventions, emphasizing their impact on the gut–brain axis and mental health. The increasing acceptance of the expanded concept of the MGB axis underscores the importance of microorganisms in mental well-being. As our understanding of the microbiome’s role in health and disease grows, probiotics emerge as promising agents for addressing mental health issues, providing new avenues for therapeutic interventions in depressive disorders.

Background: The authors of this research study intended to verify whether there are any changes in gene expression in depressed patients without coexisting inflammatory diseases for selected immune-inflammatory factors that are particularly important in autoimmune disease pathogenesis (IL-17, IL-21, IL-23, IL-35, Foxp3). Methods: The study was carried out on a group of 190 patients with depression and 100 healthy volunteers. The severity of depressive symptoms was assessed using the Hamilton Depression Scale. RT-PCR was used to evaluate mRNA expression and ELISA was used to measure protein expression of these genes. Results: The level of gene expression for IL-17, IL-21, IL-23, and IL-35 was substantially higher in the group of patients with depression compared to the control group. The mean mRNA expression of Foxp3 was considerably reduced in patients suffering from depressive disorders. There was a statistically significant correlation between the number of hospitalizations and the expression of specific inflammatory factors. Conclusions: Expression of specific inflammatory genes may be a factor in the etiopathogenesis of depressive disorders. The duration of the disease seems to be more important for the expression of the genes in question than the severity of depression. These cytokines may affect the metabolism of neurotransmitters and neuroendocrine functions in the brain as well as be a marker and a new potential therapeutic target for recurrent depressive disorders.

Depression is currently one of the most common psychiatric disorders and the number of patients receiving antidepressant treatment is increasing every year. Therefore, it is essential to understand the underlying mechanisms that are associated with higher prevalence of depression. The main component leading to the change in functioning, in the form of apathy, anhedonia, lack of motivation and sleep disturbances, is stress. This is the factor that in recent decades—due to the civilization speed, dynamic technological development as well as competitiveness and competition in relationships—significantly affects the psychophysical condition, which results in an increase in the prevalence of civilization diseases, including depression. To understand the mechanism of susceptibility to this disease, one should consider the significant role of the interaction between immune and nervous systems. Their joint development from the moment of conception is a matrix of later predispositions, both associated with the mobilization of the proinflammatory pathways (TNFα, IL-1β, IL-6) and associated with psychological coping with stress. Such an early development period is associated with epigenetic processes that are strongly marked in prenatal development up to 1 year of age and determinate the characteristic phenotype for various forms of pathology, including depression. Regarding the inflammatory hypothesis of depression, interleukin 17 (IL-17), among other proinflammatory cytokines, might play an important role in the development of depressive disorders. It is secreted by Th17 cells, crossed the placental barrier and acts on the brain structures of the fetus by increasing IL-17 receptor levels and affecting the intensity of its signaling in the brain.

Background: Experiencing stressful life events and ways of coping with them can predispose to the onset of depressive mood disorders, while depression itself can be responsible for severe stress and can weaken resilience to stressors. Thus, variables relevant to the onset of depressive episodes and the course of depression have significant relationships with coping strategies to stressors. The aim of this research was to evaluate the most commonly used stress-coping strategies in patients treated for depression compared to patients with anxiety disorders and to healthy subjects. Methods: The multidimensional coping inventory (COPE Inventory) by C. S. Carver, M. F. Scheier, and J. K. Weintraub, covering 15 stress response strategies included in more general and overarching coping styles, was used in the study. Results: Patients with depression differed from the healthy subjects in a statistically significant way. Statistical analysis showed that people with depression are less likely than healthy subjects to use Active Coping, Planning, Seeking of Instrumental and Emotional Social Support, Suppression of Competing Activities, and Positive Reinterpretation. In contrast, they are more likely to use Denial, Mental Disengagement, and Behavioral Disengagement compared to those not treated for mental disorders. The patients with depressive disorders, compared to the group of patients with anxiety disorders, scored significantly differently on stress coping strategies in only two types of actions taken in stressful situations. Conclusion: The patients with depression differed from the healthy subjects in terms of the highest number of the stress coping strategies assessed. Compared to the healthy individuals, a tendency toward an avoidant behavior style was prevalent among the depressed patients. There was no statistically significant difference between the patients with the first episode of the disease and recurrent depressive disorders in terms of stress coping strategies.

(1) Background: Only 60–70% of depressed patients respond to standard antidepressant treatments. Hence, it is essential to search for new, effective and safe therapies for unmet clinical needs of treatment-resistant depression (TRD). Agents targeting the components of the JAK-STAT signaling pathway have been shown to be relevant in immunology and are commonly used in the treatment of many hematological, rheumatological and dermatological diseases. The aim of this study was to investigate the role of elements of the JAK-STAT signaling pathway in the etiopathogenesis of depressive disorders. (2) Methods: A total of 290 subjects took part in the study (190 depressed patients, 100 healthy controls). Sociodemographic data were collected. The severity of depressive symptoms was assessed using the Hamilton Depression Rating Scale (HDRS). The gene expression at the mRNA protein levels of JAK (JAK1-JAK3) and STAT (STAT1-STAT5) was assessed by using RT-PCR and ELISA. (3) Results: Increased expression of JAK3 and decreased expression of STAT1 were observed in the group of depressed patients. (4) Conclusions: Further studies are necessary to determine whether moderation of the JAK-STAT signaling pathways is involved in the treatment of depression.

Methylphenidate (MPH) is a central nervous system stimulant that is approved and widely used for the treatment of attention-deficit hyperactivity disorder (ADHD) and narcolepsy. It acts primarily by inhibiting the reuptake of dopamine and norepinephrine, thereby enhancing synaptic concentrations of these neurotransmitters and improving attention, impulse control, and wakefulness. Despite its well-established therapeutic efficacy, MPH is associated with a complex safety profile that necessitates careful consideration, particularly in long-term use and in populations with preexisting health conditions. Cardiovascular risks, including increased heart rate, elevated blood pressure, and, in rare cases, serious adverse events such as myocardial infarction, arrhythmias, and sudden cardiac death, have been reported. Psychiatric adverse effects, including anxiety, agitation, psychotic symptoms, and exacerbation of preexisting mood disorders, also warrant close monitoring. Additionally, MPH has the potential for misuse, abuse, and dependence, particularly due to its dopaminergic effects, which can contribute to reinforcement and addiction-related behaviors. This review synthesizes current evidence on the safety of MPH, with a focus on its impact on cardiovascular and psychiatric health, and addiction potential. Special attention is given to vulnerable populations, including children, adolescents, individuals with comorbid psychiatric or cardiovascular conditions, and those with a history of substance use disorders. Furthermore, sex and gender influence health outcomes, for MPH healthcare strategies have been addressed. Given these concerns, the necessity for rigorous patient monitoring, individualized risk assessment, and adherence to prescribing guidelines is emphasized to optimize therapeutic outcomes while minimizing risks. Clinical trial number: Not applicable.