Background Purpose of study is revealing significant differences in serum proteomes in schizophrenia and bipolar disorder (BD). Results Quantitative mass-spectrometry based proteomic analysis was used to quantify proteins in the blood serum samples after the depletion of six major blood proteins. Comparison of proteome profiles of different groups revealed 27 proteins being specific for schizophrenia, and 18 – for BD. Protein set in schizophrenia was mostly associated with immune response, cell communication, cell growth and maintenance, protein metabolism and regulation of nucleic acid metabolism. Protein set in BD was mostly associated with immune response, regulating transport processes across cell membrane and cell communication, development of neurons and oligodendrocytes and cell growth. Concentrations of ankyrin repeat domain-containing protein 12 (ANKRD12) and cadherin 5 in serum samples were determined by ELISA. Significant difference between three groups was revealed in ANKRD12 concentration ( p = 0.02), with maximum elevation of ANKRD12 concentration (median level) in schizophrenia followed by BD. Cadherin 5 concentration differed significantly ( p = 0.035) between schizophrenic patients with prevailing positive symptoms (4.78 [2.71, 7.12] ng/ml) and those with prevailing negative symptoms (1.86 [0.001, 4.11] ng/ml). Conclusions Our results are presumably useful for discovering the new pathways involved in endogenous psychotic disorders. Electronic supplementary material The online version of this article (10.1186/s12864-019-5848-1) contains supplementary material, which is available to authorized users.

A total of 26 patients with depression and 20 healthy subjects were studied. Measures of apoptosis of peripheral blood lymphocytes and serum cortisol concentrations were determined. A significant increase in lymphocyte apoptosis was found in patients with depression, resulting in an increase in the proportion of lymphocytes expressing the FAS receptor; cells with morphological signs characteristic of apoptosis (nuclear condensation, vacuolization) were also seen. Changes in cellular immunity were observed on the background of clinical depressive symptomatology, with decreases in the total numbers of T-lymphocytes (CD3(+)), T-helpers (CD4(+)), and natural killer cells (CD16(+)) as compared with numbers in healthy subjects. Serum cortisol levels were elevated. Correlation analysis revealed an interaction between high cortisol levels and decreases in T-helper cells (CD4(+)) and increases in apoptosis receptor expression in patients with depressive disorder.

Background: Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal plasticity, and its dysregulation has been associated with the pathogenesis of mood and anxiety disorders. Prolactin (PRL) is a pituitary hormone which is also produced as a cytokine by immune cells and could be a neurotrophic factor regulating the functional activity of stress-related mechanisms. Aim: To investigate the possible relationship between depressive state and BDNF and PRL genotypes or levels with special reference to severity of depression. Methods: Participants of 18-70 years with a clinical diagnosis of depressive disorder of at least moderate severity were included. These patients had not been treated with antidepressant drugs before admission to hospital during the preceding period of the last 6 months, and 54.5% had never been treated with antidepressant drugs during their entire life. The DNA was genotyped for rs1341239 within the prolactin and for rs6265, rs7124442, and rs11030104 within the BDNF gene. Rs11030104 violated the Hardy-Weinberg equilibrium distribution and was excluded from further analyses. BDNF and prolactin concentration was measured in serum by MAGPIX multiplex analyzer (Luminex, USA) using MILLIPLEX ® MAP kit (Merck, Germany). Genetic associations were determined by sequentially regressing prolactin, BDNF, 17-items Hamilton's Depression (HAMD-17) and Clinical Global Impression scale, Severity (CGI-S) ratings, and depression (absent/present) on the available SNPs. Genetic associations were evaluated assuming an additive model. Results: A total of 186 depressed patients (of which 169 were women) and 94 healthy controls (67 women) were genotyped. After excluding subjects without genetic information on

AKT1 gene polymorphism rs1130214 is associated with antidepressant treatment response in patients with depressive disorders.

S. A. (2019). Investigating the potential role of BDNF and PRL genotypes on antidepressant response in depression patients: A prospective inception cohort study in treatment-free patients.