Is a cyclic neuropeptide produced primarily in the hypothalamus and plays an important neuromodulatory role for other neurotransmitter systems, with an impact on behavior, response to danger, stress, and complex social interactions, such as pair bonding and child care. This narrative expert review examines the literature on oxytocin as a brain hormone. We focused on oxytocin structure, distribution, genetics, and the oxytocin receptor system, as well as the relationship of oxytocin with other neurotransmitters and the resulting impacts on the main psychiatric disorders. Oxytocin levels have been correlated over time with mental illness, with numerous studies focusing on oxytocin and the pathophysiology of the main psychiatric disorders, such as autism, schizophrenia, personality disorders, mood, and eating disorders. We highlight the role oxytocin plays in improving symptoms such as anxiety, depression, and social behavior, as the literature suggests. Risk factors and causes for psychiatric disorders range from genetic to environmental and social factors. Oxytocin could impact the latter, being linked with other neurotransmitter systems that are responsible for integrating different situations during the development phases of individuals. Also, these systems have an important role in how the body responds to stressors or bonding with others, helping with the creation of social support groups that could speed up recovery in many situations. Oxytocin has the potential to become a key therapeutic agent for future treatment and prevention strategies concerning the main psychiatric disorders.

Transcranial direct current stimulation (tDCS) came into consideration in recent years as a promising, non-invasive form of neuromodulation for individuals suffering from mild cognitive impairment (MCI). MCI represents a transitional stage between normal cognitive aging and more severe cognitive decline, which appears in neurodegenerative diseases, such as Alzheimer’s disease. Numerous studies have shown that tDCS can have several useful effects in patients with MCI. It is believed to enhance cognitive functions, including memory and attention, potentially slowing down the progression of neurodegeneration and cognitive decline. tDCS is believed to work by modulating neuronal activity and promoting synaptic plasticity in the brain regions associated with cognition. Moreover, tDCS is generally considered safe and well-tolerated, making it an attractive option for long-term therapeutic use in MCI. However, further research is needed to determine the optimal stimulation parameters and long-term effects of tDCS in this population, as well as its potential to serve as a complementary therapy alongside other interventions for MCI. In this review, we included 16 randomized clinical trials containing patients with MCI who were treated with tDCS. We aim to provide important evidence for the cognitive enhancement using tDCS in patients with MCI, summarizing the effects and conclusions found in several clinical trials, and discuss its main mechanisms.

The memory-enhancing activity of Matricaria chamomilla hydroalcoholic extract (MCE) is already being investigated by behavioral and biochemical assays in scopolamine-induced amnesia rat models, while the effects of scopolamine (Sco) on cerebral glucose metabolism are examined as well. Nevertheless, the study of the metabolic profile determined by an enriched MCE has not been performed before. The present experiments compared metabolic quantification in characteristic cerebral regions and behavioral characteristics for normal, only diseased, diseased, and MCE- vs. Galantamine (Gal)-treated Wistar rats. A memory deficit was induced by four weeks of daily intraperitoneal Sco injection. Starting on the eighth day, the treatment was intraperitoneally administered 30 min after Sco injection for a period of three weeks. The memory assessment comprised three maze tests. Glucose metabolism was quantified after the 18F-FDG PET examination. The right amygdala, piriform, and entorhinal cortex showed the highest differential radiopharmaceutical uptake of the 50 regions analyzed. Rats treated with MCE show metabolic similarity with normal rats, while the Gal-treated group shows features closer to the diseased group. Behavioral assessments evidenced a less anxious status and a better locomotor activity manifested by the MCE-treated group compared to the Gal-treated group. These findings prove evident metabolic ameliorative qualities of MCE over Gal classic treatment, suggesting that the extract could be a potent neuropharmacological agent against amnesia.

Background: Brain-derived neurotrophic factor (BDNF) and oxytocin (OXT) have been independently implicated in the pathophysiology of major depressive disorder (MDD), yet few longitudinal studies have examined their concurrent modulation during early antidepressant treatment. This study investigated changes in plasma BDNF and oxytocin concentrations over the first four weeks of pharmacological treatment in patients with unipolar MDD and explored their association with changes in depressive symptom severity. Methods: Twenty-six medication-free patients with unipolar major depressive disorder were assessed at baseline, before antidepressant initiation, and after four weeks of treatment. Depressive severity was measured using the 17-item Hamilton Depression Rating Scale (HAMD-17). Plasma BDNF and oxytocin concentrations were quantified using enzyme-linked immunosorbent assay kits (ELISA). Within-subject changes were analysed using the Wilcoxon signed-rank test, and associations between changes in clinical severity and biomarker levels were examined using Spearman’s rank correlation coefficients. Results: Depressive symptom severity significantly decreased after four weeks of treatment. Plasma BDNF and oxytocin levels also demonstrated significant changes over the same period. A moderate negative correlation was observed between reductions in HAMD-17 scores and the change in BDNF concentrations (ρ = −0.554, p = 0.003), indicating that greater clinical improvement was associated with greater increases in plasma BDNF levels. A moderate positive correlation was found between changes in depressive severity and changes in oxytocin concentrations (ρ = 0.414, p = 0.035). No statistically significant differences in biomarker changes were observed across antidepressant classes; however, these subgroup analyses should be interpreted cautiously given the limited sample sizes in each treatment subgroup. Conclusions: Early antidepressant treatment in unipolar MDD is accompanied by modulation of peripheral neurotrophic and neuropeptidergic markers. The association between symptom improvement and BDNF dynamics supports the relevance of neuroplasticity-related mechanisms during early treatment, while oxytocin alterations may reflect parallel adaptation within stress-regulatory systems. Larger longitudinal studies are required to clarify the predictive and mechanistic significance of these findings.