This research aimed to investigate factors associated with vitamin D deficiency and to provide data about its prevalence in patients suffering from different psychiatric illnesses. The study had a cross-sectional design and it included 220 patients of both genders, aged from 19-81 y, with a wide range of mental disorders (F00-F89), and treated in routine ambulatory and hospital practice. The researchers collected data from three sources: medical records, a study questionnaire and biochemical analysis of patients’ serum samples (concentration of vitamin D measured as 25(OH)D, calcium, phosphorus, magnesium, sodium and potassium). Data were analyzed using descriptive statistics, methods for hypothesis testing and binary logistic regression, at the p≤0.05 level. A total of 140 patients (64%) had a deficiency of vitamin D (20 ng/mL). Among variables related to demographics, life style habits, mental illness, comorbid disorders and drugs, two of them, female gender (odds ratio (OR)=2.5, 95% confidence interval (CI)=1.3-4.9, p=0.006) and using clozapine (OR=15.6, 95% CI 1.7-144.7, p=0.02), were significantly associated with vitamin D deficiency. Physical activity (OR= 0.4, 95% CI 0.2-0.9, p=0.02), exercising (OR=0.2, 95% CI <0.1-0.7, p=0.02) and offal in the diet (OR=0.5, 95% CI 0.3-0.9, p=0.03) significantly aggregated in the patients who had a 25(OH)D serum concentration above the deficiency cut-off level. Patients with mental disorders are at high risk for vitamin D deficiency, particularly females and clozapine users as well as those having no adequate physical activity or dietary habits.

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.

Turner syndrome is a genetic disorder that affects only females. It has specific cognitive characteristics, but speech and language data are scarce.Prospective case report; we report a girl aged se...

The increasing and global distribution of microplastics and nanoplastics (MPs/NPs) in the environment has led to concern about their potential influence on human health, especially on the gastrointestinal tract, as well as the brain. MPs/NPs could traverse epithelial and endothelial barriers, disrupt the gut microbiota, and perturb the microbiota–gut–brain axis, leading to systemic inflammation and possibly extending neurodegenerative processes. Experimental models now demonstrate that MPs/NPs reprogram nuclear and mitochondrial epigenetics—DNA methylation, histone modifications, non-coding RNAs, and mitochondrial DNA regulation—in gut, immune, and neural cells with downstream effects on synaptic function, neuronal survival, and protein aggregation. This mechanistic narrative review integrates preclinical and emerging human evidence of how MPs/NPs compromise intestinal barrier integrity, modulate gut microbiota composition, affect the blood–brain barrier, and converge on oxidative stress, neuroinflammatory signaling, and cell death pathways within the central nervous system across key neurodegenerative diseases. Overall, the review offers an integrated model in which environmental exposure to chronic MPs/NPs disrupts the microbiota–gut–brain axis and drives concurrent nuclear and mitochondrial epigenetic remodeling, lowering the threshold for neurodegeneration in susceptible individuals, while outlining candidate mechanistic readouts that require exposure-specific validation in human-relevant models and longitudinal cohorts.

Schizophrenia is a chronic mental illness with a poor quality of life (QoL). The main aim of this study was to measure the QoL and factors that affect the QoL of patients with schizophrenia placed in a social welfare institution. This cross-sectional study included 287 patients with schizophrenia who were treated in a long-stay social care institution in which QoL was assessed using five different instruments: the World Health Organization Quality of Life scale, the EuroQoL Five-Dimension-Five-Level scale (including the visual analog scale), the Quality of Life Enjoyment and Satisfaction Questionnaire – Short Form, and the Brief Psychiatric Rating Scale. To determine the impact of patients’ characteristics on score values, multiple linear regression using backward elimination was employed. Due to non-normality in the distribution of the dependent variables, a Box–Cox power transformation was applied to each dependent variable prior to conducting multiple linear regression analysis. Results revealed that patients with schizophrenia have lower QoL. Our study revealed that age, level of education, type of accommodation, type of pavilion, age of onset of the disease, number of prescribed antipsychotics, number of psychiatric comorbidities, duration of therapy, and the number of daily doses of antipsychotics are dominant contributors to the QoL in patients with schizophrenia who were treated in social welfare institution.