Electroconvulsive therapy (ECT) remains one of the most effective interventions for treatment-resistant psychiatric disorders, particularly major depressive disorder and bipolar disorder. Despite extensive clinical and preclinical investigations, the precise neurobiological mechanisms underlying ECT’s therapeutic effects are not fully understood. This review explores the molecular and cellular pathways involved in ECT, emphasizing its impact on neurotrophic signaling, oxidative stress, apoptosis, and neuroplasticity. Evidence suggests that ECT modulates brain-derived neurotrophic factor and other neurotrophic factors, promoting synaptic plasticity and neuronal survival. Additionally, ECT influences the hypothalamic–pituitary–adrenal axis, reduces neuroinflammation, and alters neurotransmitter systems, contributing to its antidepressant effects. Recent findings also highlight the role of mitochondrial function and oxidative stress regulation in ECT-induced neural adaptation. By synthesizing current molecular insights, this review provides a comprehensive perspective on the neurobiological mechanisms of ECT, offering potential directions for future research and therapeutic advancements in brain stimulation.

Background: Insomnia is markedly more prevalent in rheumatoid arthritis (RA) patients than in the general population and is closely linked to pain, fatigue, psychological comorbidities, and systemic inflammation. Evidence suggests a bidirectional relationship, where active disease worsens sleep quality, while poor sleep amplifies inflammatory activity and symptom severity. Methods: A narrative review was conducted using PubMed, Scopus, Web of Science, and Embase to identify studies from the last 15 years involving adult RA patients. Inclusion criteria required assessment of insomnia or sleep quality in relation to disease activity, treatment outcomes, or inflammatory markers. Data from clinical trials, cohort studies, and reviews were synthesized to examine prevalence, mechanisms, and therapeutic implications. Results: Insomnia affects up to 45% of RA patients and correlates with higher DAS28 scores, elevated CRP/ESR, increased pain sensitivity, and reduced quality of life. Contributing factors include chronic pain, stiffness, elevated IL-6 and TNF-α, depression, anxiety, and medication side effects. Conventional DMARDs, corticosteroids, and biologics indirectly improve sleep via inflammation control, with IL-6 inhibition showing potential sleep-specific benefits. Psychotropic agents may help in comorbid depression/anxiety but are best combined with cognitive behavioral therapy for insomnia (CBT-I). Conclusions: Insomnia is a prevalent, multifactorial problem in RA that adversely affects disease activity, symptom burden, and functional outcomes. Integrating sleep evaluation into routine RA management and adopting interdisciplinary strategies that address both inflammation and sleep disturbance may enhance patient outcomes. High-quality longitudinal studies using objective sleep measures are needed to clarify causal relationships and optimize therapy.

Background: This cross-sectional study aimed to assess the correlation between subjective oral health status and mental health in a group of university students in Serbia. Methods: The study included 948 students, aged between 18 and 27, from the Faculty of Medical Sciences, University of Kragujevac, Serbia, and was conducted in 2020. The World Health Organization’s Oral Health Questionnaire for Adults was utilized to evaluate the respondents’ self-perceived oral health and oral hygiene practices. The existence of depressive symptoms was evaluated using the Beck Depression Inventory-II (BDI-II), and the Zung self-rating anxiety scale (SAS) was used for determining anxiety symptoms. Results: It is observed that 28.9% of respondents exhibit symptoms of depression and 42.3% showed symptoms of anxiety. Results show that students with severe depression and anxiety symptoms very often reported lower self-perceived oral health and oral health problems. Although the nature of this relationship has not been thoroughly evaluated, several studies have shown a mutually dependent connection between oral health and mental health. Conclusions: The results suggest that some aspects of oral health are associated with higher risks of developing symptoms of depression or anxiety, and vice versa.

Background and Objectives: The objective of the study is to determine whether there is a difference in physical therapy outcomes in patients with cervical and/or lumbar pain who have insomnia compared to patients without insomnia during a two-week period of active treatment under the conditions of routine clinical practice. Materials and Methods: The study population consisted of two groups of subjects with chronic back pain, a group with insomnia (“case”) with a total of 38 subjects and a control group without insomnia (“control”) with a total of 41 subjects, who filled out a set of measurement questionnaires: the McGill Pain Questionnaire and its short form (SF-MPQ), the Insomnia Severity Index (ISI) and the European Quality of Life Questionnaire of Life (Euro Qol; EQ-5D). Determination of the biomarkers of structural damage to the nervous tissue, neurofilament polypeptide (NEF—neurofilament polypeptide), neuron-specific enolase (NSE—neuron-specific enolase) and protein S100B was performed by measuring their concentrations in the blood using the ELISA method (enzyme immunosorbent assay). Statistical analysis of the collected data included a descriptive analysis, hypothesis testing methods and univariable and multivariable regression models. Results: At the end of the treatment visits, the level of pain remained higher in some subjects of the experimental group, but the statistical significance of the baseline difference disappeared because of the higher relative treatment response in the controls. Measured with a visual analogue scale, the treatment improved the patients’ quality of life much more in experimental than control subjects, as is proven by the statistically significant difference for the percent change from baseline (~31% vs. ~14%). At baseline, all three neurotropic biomarkers had significantly higher serum values in the subjects of the experimental group than in the control patients, which suggested more damage to the neuronal structures. During the treatment course, their serum concentrations decreased, from 36% to 95%, but for S100B, unlike NES and NEF, there was no statistically significant difference between the study groups at the end of the treatment visits. Conclusions: The results of the study have immediate scientific and practical significance because they contribute to new knowledge about the place and role of insomnia in patients with cervical and/or lumbar pain who are treated with physical medicine methods in the conditions of routine clinical practice. The treatment of insomnia should be an indispensable part of therapeutic treatment for patients with back pain.

Electroconvulsive therapy (ECT) remains one of the most effective interventions for treatment-resistant psychiatric disorders, particularly major depressive disorder and bipolar disorder. Despite extensive clinical and preclinical investigations the precise neurobiological mechanisms underlying ECT’s therapeutic effects are not fully understood. This review explores the molecular and cellular pathways involved in ECT, emphasizing its impact on neurotrophic signaling, oxidative stress, apoptosis, and neuroplasticity. Evidence suggests that ECT modulates brain-derived neurotrophic factor (BDNF) and other neurotrophic factors, promoting synaptic plasticity and neuronal survival. Additionally, ECT influences the hypothalamic-pituitary-adrenal (HPA) axis, reduces neuroinflammation, and alters neurotransmitter systems, contributing to its antidepressant effects. Recent findings also highlight the role of mitochondrial function and oxidative stress regulation in ECT-induced neural adaptation. By synthesizing current molecular insights, this review provides a comprehensive perspective on the neurobiological mechanisms of ECT, offering potential directions for future research and therapeutic advancements in brain stimulation.

Major depressive disorder (MDD) continues to be a primary cause of disability globally, with a significant number of patients exhibiting resistance to standard pharmacological and psychotherapeutic interventions. In recent years, non-invasive brain stimulation techniques, especially transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS), have emerged as promising therapies for treatment-resistant MDD. A comprehensive search was performed in PubMed, which included all studies published over the last ten years. Eligible studies encompassed both animal models and clinical investigations. This review provides a comparative overview of transcranial electrical stimulation modalities, with a focus on their mechanisms of action, clinical efficacy, and underlying neurobiological mechanisms. We pay particular attention to the role of the neurotrophin system, specifically brain-derived neurotrophic factor (BDNF), in mediating the treatment effects of transcranial stimulation. Recent findings indicate that neuromodulation could improve neuroplasticity by increasing BDNF levels and associated signaling pathways, which may help stabilize mood and enhance the improvement of individuals with MDD. A more profound understanding of these mechanisms could lead to more precise, biomarker-driven interventions. Further research is essential to elucidating the long-term effects of brain stimulation on neurotrophin levels and to creating more individualized treatment strategies.