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Major depressive disorder (MDD) remains the subject of ongoing research as a multifactorial disease and a serious public health problem. There is a growing body of literature focusing on the role of neurotrophic factors in pathophysiology of MDD. A neurotrophic hypothesis of depression proposes that abnormalities of neurotrophins serum levels lead to neuronal atrophy and decreased neurogenesis, resulting in mood disorders. Consequently, in accordance with recent findings, antidepressant treatment modifies the serum levels of neurotrophins and thus leads to a clinical improvement of MDD. The purpose of this review is to summarize the available data on the effects of various antidepressants on serum levels of neurotrophins such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor (IGF-1). In addition, the authors discuss their role as prognostic factors for treatment response in MDD. A literature search was performed using the PubMed database. Following the inclusion and exclusion criteria, nine original articles and three meta-analyses were selected. The vast majority of studies have confirmed the effect of antidepressants on BDNF levels. Research on IGF-1 is limited and insufficient to describe the correlation between different antidepressant drugs and factor serum levels; however, four studies indicated a decrease in IGF-1 after treatment. Preliminary data suggest BDNF as a promising predictor of treatment response in MDD patients. The role of IGF-1 needs further investigation.

BackgroundThe potential dynamics of cognitive impairment in schizophrenia is discussed in the literature of the field. Recent publications suggest modest changes in level of cognitive impairment after first psychotic episode. Present article attempts to explore cognitive differences between patients and controls across age groups and differences between age groups in clinical group.MethodsOne hundred and twenty-eight hospitalized patients with schizophrenia (64 women and 64 men) and 68 individuals from the control group (32 women and 32 men) aged 18–55 years were examined. The patients were divided into age groups (18–25, 26–35, 36–45, 46–55). Both groups were examined using Wisconsin Card Sorting Test, Rey Auditory Verbal Learning Test, Rey Osterrieth Complex Figure Test, Trail Making Test (A and B), Stroop Test, verbal fluency test and Wechsler digit span.ResultsPatients with schizophrenia obtained significantly lower scores versus the control group in regard to all the measured cognitive functions (Mann–Whitney U; p < 0.05. Most deficits were present in all age groups, however, statistically important impairment in executive functions (WCST) were present only in “older” groups.ConclusionsPatients with schizophrenia obtained less favourable results than the control group in all age groups. Deficits regarding executive functions do not seem to be at a significant level among the youngest group, whereas they are more noticeable in the group of 46–55-year-olds. Executive functions are significantly lowered in the group aged 36–45 in comparison to the “younger” groups. The level of cognitive functions shows a mild exacerbation in connection with age, whereas cognitive rigidity proved to be related to the number of years spent without hospital treatment.

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Major depressive disorder (MDD) is one of the most prevalent mental illness and a leading cause of disability worldwide. Despite a range of effective treatments, more than 30% of patients do not achieve remission as a result of conventional therapy. In these circumstances the identification of novel drug targets and pathogenic factors becomes essential for selecting more efficacious and personalized treatment. Increasing evidence has implicated the role of inflammation in the pathophysiology of depression, revealing potential new pathways and treatment options. Moreover, convergent evidence indicates that MDD is related to disturbed neurogenesis and suggests a possible role of neurotrophic factors in recovery of function in patients. Although the influence of antidepressants on inflammatory cytokines balance was widely reported in various studies, the exact correlation between drugs used and specific cytokines and neurotrophins serum levels often remains inconsistent. Available data suggest anti-inflammatory properties of selective serotonin reuptake inhibitors (SSRIs), selective serotonin and noradrenaline inhibitors (SNRIs), and tricyclic antidepressants (TCAs) as a possible additional mechanism of reduction of depressive symptoms. In this review, we outline emerging data regarding the influence of different antidepressant drugs on a wide array of peripheral biomarkers such as interleukin (IL)-1ß, IL-2, IL-5, IL-6, IL-8, IL-10, C-reactive protein (CRP), or interferon (IFN)-γ. Presented results indicate anti-inflammatory effect for selected drugs or lack of such effect. Research in this field is insufficient to define the role of inflammatory markers as a predictor of treatment response in MDD.