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Background Neurotrophin-4/5 (NT-4/5) and glutathione peroxidase-1 (GPX-1) have been shown to play a major role in neuronal processes including depression and posttraumatic stress disorder (PTSD). They protect the body from oxidative damage by affecting neuronal growth, development and plasticity. The aim of the study was to evaluate the concentrations of NT-4/5, GPX-1, tumor necrosis factor-α (TNF-α), and l -arginine in patients suffering from varying levels of depression severity, PTSD, and depression comorbid with PTSD. Methods The study involved 460 participants, 360 of whom were diagnosed with different types of depressive episodes. They included: 60 patients with mild depression (MD), 60 patients with moderate depression (MOD), 60 patients with severe depression (SeD), 60 patients with MD and PTSD (MD + PTSD), 60 patients with MOD and PTSD (MOD + PTSD), 60 patients with SeD and PTSD (SeD + PTSD), and 60 patients with PTSD alone. Each group of 60 subjects comprised 30 females and 30 males. The control group comprised 40 subjects. The 10th revision of the International Statistical Classification of Diseases and Related Health Problems was utilized to diagnose depression and PTSD. At 7 a.m. blood samples were collected and serum NT-4/5, GPX-1, TNF-α and l -arginine concentrations were assessed using the ELISA method. Results Depressive episodes with and without PTSD and PTSD alone became more severe as the levels of TNF-α, l -arginine increased and the levels of NT-4/5, GPX-1 decreased. Conclusion l -arginine, TNF-α, NT-4/5 and GPX-1 can be markers of depression severity in both males and females with first depressive episode with or without posttraumatic stress disorder.

Background Disrupted circadian rhythm of melatonin secretion in depression shows a relationship with the exacerbation of inflammatory processes. Proinflammatory mechanisms of depression are sustained by oxidative stress. This contributes to melatonin deficiency and to the malfunction of the defense mechanisms in the brain. Disrupted melatonin secretion in depression may have an influence on the concentrations of neurotrophic factors (NF), such as neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). Disturbance in neurotrophin release may affect synaptic plasticity and cause exacerbation of neurodegenerative processes in the central nervous system. The aim of this study was to assess the concentrations of melatonin and NF of the brain in patients with varying levels of depression severity. Method 160 males and females were enrolled in the study, 120 of whom were diagnosed with various types of depression. The control group comprised 40 healthy individuals. At 3:00 a.m. all patients had salivary melatonin concentrations determined utilizing a competitive enzyme immunoassay technique (ELISA). In addition, at 7:00 a.m. all patients had serum neurotrophin (NT-3, BDNF, NGF) concentrations determined by means of ELISA. Results The highest melatonin secretion was observed at 3:00 a.m. in severely depressed females. In the groups with mild and moderate depression, melatonin secretion at 3:00 a.m. was comparable between males and females. In addition, a decrease in the concentrations of neurotrophins was revealed in patients at all levels of depression severity. Conclusion Melatonin may be a significant marker of depression severity. Melatonin and NF in depressed patients show neuroprotective effects.

Background Both major depression and posttraumatic stress disorder (PTSD) are characterized by inflammation, increased concentration levels of proinflammatory cytokines, decreased neurogenesis followed by neuroprogression, as well as mitochondrial and the hypothalamic-pituitary-adrenal axis dysfunction. Elevated levels of oxidative stress caused by an increased activity of prooxidants over antioxidants are also observed. Based on several reports, depressive episodes can lead to the sensitization of immune-inflammatory pathways. Thus, depression, PTSD, and depression comorbid with PTSD are associated with immune-inflammatory markers. The study aimed at evaluating concentration levels of iNOS, HO-1, IL-33, and MIP-1β in depression with and without PTSD. Methods A total number of participants enrolled in the study was 460. Out of them, 420 subjects with various levels of depression severity constituted the study group (210 males and 210 females), and 40 subjects (20 males and 20 females) constituted the control group. Each study group comprised 60 patients (30 males and 30 females) with mild depression (MD), moderate depression (MOD), severe depression (SeD), MD and PTSD (MD + PTSD), MOD and PTSD (MOD + PTSD), SeD and PTSD (SeD + PTSD), and with PTSD alone. At 7:00 a.m., all patients had serum concentrations of iNOS, HO-1, IL-33, MIP-1β determined using ELISA. Results Both depression exacerbation and PTSD comorbidity led to elevated levels of iNOS, HO-1, IL-33, and MIP-1β. Conclusion Depression both with and without PTSD leads to elevated levels of inflammation and an oxidant/antioxidant imbalance. Alterations in both cytokines and oxidative stress are related to the mechanisms responsible for the development of depressive symptoms.

Development of depression is associated with the body's response to prolonged stress, which adversely affects the functioning of the nervous, endocrine and immune systems. Prolonged stress can lead to the development of a so-called allostatic load and reduction of concentration of brain-derived neurotrophic factor. These changes result in impairment of neurogenesis and synaptic remodeling process. This article illustrates the involvement of key mediators of allostasis such as the neuroendocrine and immune systems, in the pathogenesis of depression. The literature concerning the contribution of the neuroendocrine and immune systems to depression incidence was reviewed. Development of depression is associated with disturbance of the body's allostasis and inflammatory activation of the immune system. It leads to a chronic increase in the concentration of cortisol and proinflammatory cytokines, which results in an allostatic load. This load leads to neurodegeneration, eventually causing irreversible cognitive impairment and permanent disability. Determination of the concentration of chemokines and their receptors is an important indicator of activation of the immune and neuroendocrine systems. The activity of these systems reflects the severity of the disease and provides important information for effective antidepressant treatment.

Background Depression can be perceived as a psychoneuroimmunological disorder in which cytokines affecting the body's neurochemical and neuroendocrine functions play an important role. Among cytokines, chemokines participating in activation of the inflammatory response are considered to be crucial. Methods 160 men and women were enrolled in the study. 120 of them were diagnosed with various types of depression. The mean age was 45.2 ± 4.5 years (range: 19–47 years). The control group consisted of 40 healthy individuals. The average age in this group was 42.4 ± 4.1 years. Plasma levels of chemokines and their receptors (CCL-5 – RANTES and CXCR-5, SDF-1 and CXCR-4), as well as of IL-6, were assessed by ELISA. Results There was an increase in SDF-1 and CCL-5 levels in women and men with different severities of depression, versus the control group. Also, an increase in the IL-6 levels, CXCR4 and CCR-5 receptors was observed in both women and men with all types of depression. Levels of SDF-1 and CCL-5 chemokines, as well as of CCR-5 and CXCR4 chemokine receptors, were higher in women than in men. Conclusions The results of this study indicate the need for assessment of CCL-5 and SDF-1 chemokines levels, as they are likely markers of developing depression. Early measurement of these chemokines levels may be helpful in choosing the best pharmacotherapy.

Patients with schizophrenia are predisposed toward developing cardiovascular disease. Although neuroleptics affect the cardiovascular system, it is also important to consider the consequences of the disease itself such as lower physical activity due to living on disability pension, inadequate nutrition, and/or nicotine addiction, being more common among patients with schizophrenia versus the general population. All these factors combined lead to an increased risk of death caused by cardiovascular conditions in schizophrenic patients. Individuals receiving typical antipsychotic drugs have been reported to have elevated concentrations of antiphospholipid antibodies, including anticoagulants and anticardiolipin antibodies. The presence of both antibodies is associated with an increased risk for thromboembolism. It is also likely that mental illness is accompanied by increased procoagulant activity. Patients with acute psychosis have been shown to have a statistically significant increase in the concentrations of D-dimer, P-selectin, and in the expression of platelet glycoprotein IIb/IIIa receptors. Learning about causes and mechanisms of venous thromboembolism could help to reduce or neutralize the adverse effects of antipsychotic treatment and facilitate the identification of appropriate markers necessary to monitor changes and provide preventive care against hazardous and potentially fatal complications such as deep venous thrombosis and pulmonary embolism. Before atypical neuroleptic treatment is administered to hospitalized patients, all possible risk factors for thromboembolism should be considered to allow the application of lower risk drugs. Also, other preventive measures should be taken into account, including hydration, compression stockings, regular exercise of lower extremities, and low-molecular-weight heparin injections.

Background Stress may induce inflammatory changes in the immune system and activate pro-inflammatory cytokines and their receptors by activating the hypothalamic–pituitary–adrenal axis. Methods 460 hospitalized patients with panic disorders (PD) and/or personality disorders (P) were studied. The study group comprised subjects with PD, avoidant personality disorder (APD), borderline personality disorder (BPD), obsessive-compulsive personality disorder (OCPD), and concomitant (PD + APD; PD + BPD; PD + OCPD). Each study group consisted of 60 subjects (30 females and 30 males). The control group included 20 females and 20 males without any history of mental disorder. ELISA was used to assess the levels of chemokines: CCL-5/RANTES (regulated on activation, normal T-cell expressed and secreted), CXCL-12/SDF-1 (stromal derived factor), their receptors CXCR-5 (C-C chemokine receptor type-5), CXCR-4 (chemokine C-X-C motif receptor-4), and IL-6. Results Statistically significant differences in the levels of CCL-5 and CCR-5 were revealed between all study groups. The greatest differences were found between the groups with PD + OCPD and PD + APD. Moreover, concomitance of PD with P significantly increased the level of chemokines and their receptors in all study groups versus the subjects with P alone. Conclusions The results of the study show differences between the groups. To be specific, inflammatory markers were more elevated in the study groups than the controls. Therefore, chemokines and chemokine receptors may be used as inflammatory markers in patients with PD co-existent with P to indicate disease severity. PD was found to be a factor in maintaining inflammatory activity in the immune system in patients with P.

Introduction The co-occurrence of generalized anxiety disorder and personality disorders suggests the existence of association between the neurobiological predispositions leading to the development of these disorders and activation of cytokine system. Pro-inflammatory chemokines such as CCL-5/RANTES (regulated upon activation normal T cell expressed and secreted) and CXCL12/SDF-1 (stromal derived factor) play an important role in immune response. Methods A total of 160 participants were enrolled in the study, 120 of whom comprised the study group (people with the dual diagnosis of personality disorder and generalized anxiety disorder). The mean age was 41.4 ± 3.5 years (range: 20–44 years). The control group consisted of 40 healthy individuals in the mean age of 40.8 ± 3.1 years (range: 20–43 years). A blood sample was collected from each participant and the plasma levels of the CCL-2/MCP-1 (monocyte chemoattractant protein-1), RANTES and SDF-1 chemokines were determined by ELISA. Results Increased levels of MCP-1 and SDF-1 were found both in women and in men versus the control group for all types of personality disorders. The levels of CCL-5 in men were significantly increased versus the control group and significantly higher in women than in men. Neither women nor men with avoidant or obsessive-compulsive personality disorder showed any significant differences in MCP-1 or SFD-1 levels. In subjects with borderline personality disorder, the levels of the study chemokines were higher in women than in men. Conclusions Our study has shown the need for determination of proinflammatory interleukins which are considered as biomarkers of personality disorders and generalized anxiety disorders.

Human sexuality is contingent upon many biological and psychological factors. Such factors include sexual drive (libido), physiological arousal (lubrication/erection), orgasm, and ejaculation, as well as maintaining normal menstrual cycle. The assessment of sexual dysfunction can be difficult due to the intimate nature of the problem and patients’ unwillingness to discuss it. Also, the problem of dysfunction is often overlooked by doctors. Atypical antipsychotic treatment is a key component of mental disorders’ treatment algorithms recommended by the National Institute of Health and Clinical Excellence, the American Psychiatric Association, and the British Society for Psychopharmacology. The relationship between atypical antipsychotic drugs and sexual dysfunction is mediated in part by antipsychotic blockade of pituitary dopamine D2 receptors increasing prolactin secretion, although direct correlations have not been established between raised prolactin levels and clinical symptoms. Variety of mechanisms are likely to contribute to antipsychotic-related sexual dysfunction, including hyperprolactinemia, sedation, and antagonism of a number of neurotransmitter receptors (α-adrenergic, dopaminergic, histaminic, and muscarinic). Maintaining normal sexual function in people treated for mental disorders can affect their quality of life, mood, self-esteem, attitude toward taking medication, and compliance during therapy.