Serum Of Schizophrenia Patients Research Articles

Diagnostic significance and potential function of miR-320d in schizophrenia.

Schizophrenia is a chronic brain disorder and needs objective diagnostic biomarkers. MicroRNAs are highly expressed in the nervous system. The study investigated the expression and clinical values of serum miR-320d in schizophrenia patients. In addition, the underlying mechanism was preliminarily examined via bioinformatic analysis. Serum samples were collected from 57 patients with first-episode schizophrenia and 62 healthy controls. The cognitive function of patients was assessed via Measurement and Treatment Research to Improve Cognition in Schizophrenia Consensus Cognitive Battery (MCCB) consisting of seven domains. Serum miR-320d levels were tested via qRT-PCR. The miRNA target predictions were obtained from Target Scan, and annotated through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Based on the GSE167630 dataset, downregulated serum miR-320d in schizophrenia was identified, which was determined in the serum of schizophrenia patients. Serum miR-320d presented a conspicuous relationship with MCCB score in both the control group and the schizophrenia group. After adjusting for age, sex, BMI, and education, serum miR-320d was still independently related to the occurrence of schizophrenia. It can identify schizophrenia cases from healthy ones with an AUC of 0.931. The Go enrichment analysis indicated that the target genes were mainly enriched in homophilic cell adhesion and cell-cell adhesion via plasma-membrane adhesion molecules, and GTPase activity and guanosine diphosphate (GDP) binding. Rap1 signaling pathway was enriched via KEGG analysis. Serum miR-320d can be taken as a candidate marker for the diagnosis of schizophrenia. Its regulatory role in neuronal cell adhesion and Rap1 signaling pathway might be the potential underlying mechanism of miR-320d in schizophrenia.

Salivary Galectin 3 Levels in Schizophrenia Patients.

To compare the levels of galectin 3 in the serum and saliva of patients with schizophrenia and normal subjects. Cross-sectional analytical study. Place and Duration of the Study: Physiology Department and Multifunctional Research Lab of Islamic International Medical College, in association with the Institute of Psychiatry Benazir Bhutto Hospital, Rawalpindi, from September 2022 to May 2023. There were 60 subjects in this study which included 30 Schizophrenia patients and 30 age and gender aligned healthy subjects. Clinically diagnosed patients of schizophrenia as per standards of diagnoses given in Diagnostic and Statistical Manual of Mental Disorders (fifth edition) were included. Unstimulated whole-mouth saliva was collected through the spitting method from the study subjects. Tetra acetic acid (EDTA) tubes were used to collect blood samples and to measure the association of galectin-3 between saliva and serum of schizophrenia patients. Enzyme linked immunosorbent assay (ELISA) was performed. Independent samples t-test and Pearson correlation were implemented. Mean salivary galectin 3 level were far more significant in schizophrenia patients as opposed to their healthy subjects having CI 95% (641.51 and 822.45, p-value <0.001). A positive association was observed between salivary and serum levels of galectin 3 in schizophrenia patients (p = 0.03). Galectin 3 levels are raised in the saliva of schizophrenia patients and these levels are positively correlated with levels of galectin 3 in the serum of schizophrenia patients. Galectin 3 levels in the saliva can be an effective indicator in diagnostic confirmation of clinically suspected schizophrenia patients. Galectin 3, Schizophrenia, Saliva, Serum level, Inflammation.

Lactate levels in the brain and blood of schizophrenia patients: A systematic review and meta-analysis

BackgroundThe pathophysiological mechanisms of schizophrenia are still unclear. Converging evidence suggests that energy metabolism abnormalities are involved in schizophrenia, and support its role in the pathophysiology of this disease. Lactate plays an important role in energy metabolism. Many studies have reported changes in the levels of lactate in the brain and serum of schizophrenia patients; however, the results from these studies are not consistent. To overcome this limitation, the goal of the present meta-analysis is to analyze the changes in lactate levels in the brain and blood of schizophrenia patients. MethodsFor this systematic review and meta-analysis, we performed a thorough search of relevant literature in the English language, using the MEDLINE, Cochrane, and Embase databases. ResultsIn the present meta-analysis, 20 studies were scrutinized, including 13 studies on brain lactate levels, which involved 322 schizophrenia patients and 324 healthy individuals as controls. 7 studies on blood lactate levels, involving 234 schizophrenia patients and 238 healthy individuals, were also included. Brain lactate levels were elevated in schizophrenia patients, both in vivo and in post-mortem studies. Nevertheless, blood lactate levels in schizophrenia patients have revealed no statistically significant difference, as compared with control individuals. ConclusionsIn comparison with healthy individuals, schizophrenia patients had higher lactate levels in the brain, rather than in the blood. These findings suggest independent regulatory mechanisms of lactate levels in the brain and peripheral tissues. Abnormal lactate metabolism in the brain may be an important pathological mechanism in schizophrenia.

DNA-hydrolyzing catalytic IgGs from schizophrenia patients do not affect cell viability of the SH-SY5Y human neuroblastoma cell line

IntroductionDNA-hydrolyzing catalytic IgGs have caspase-dependent cytotoxic effects in autoimmune diseases. Recently, DNA-hydrolyzing IgGs have been discovered in schizophrenia. However, their cytotoxic properties have not been studied.ObjectivesTo assess the effect of serum IgGs with DNA-hydrolyzing activity of schizophrenia patients on the cell viability of the SH-SY5Y human neuroblastoma cell line.MethodsSerum of 8 patients with paranoid schizophrenia in the acute phase and 7 mentally and somatically healthy persons were used. IgG was purified from serum by affinity chromatography on Protein-G-Sepharose columns. The DNA hydrolyzing activity of IgG was assessed by the degree of hydrolysis of the pBluescript plasmid. The cell viability of the SH-SY5Y human neuroblastoma cell line after exposure to purified IgG preparations was assessed by high-throughput screening on the CellInsight CX7 platform (Thermo Scientific, USA) using the fluorescent dyes propidium iodide and Hoechst.ResultsOf the 8 IgG preparation obtained, 4 drugs had high DNA-hydrolyzing activity. All tested IgG preparations from healthy donors were inactive. One-way ANOVA analysis of the proportion of dead cells of the SH-SY5Y line after exposure to antibodies (0.1 mg/ml) showed no significant differences in the proportion of dead cells (p=0.688 after 24 hours; p=0.831 after 48 hours). Similar results were obtained at a higher concentration of antibodies - 0.2 mg/ml.ConclusionsThus, it has been shown in vitro that IgGs isolated from the serum of schizophrenia patients with or without DNA-hydrolyzing activity does not exhibit cytotoxic properties against the SH-SY5Y human neuroblastoma cell line. Support by Grant of RSF № 18-15-00053P.DisclosureNo significant relationships.

Searching for biomarkers in schizophrenia and psychosis: Case-control study using capillary electrophoresis and liquid chromatography time-of-flight mass spectrometry and systematic review for biofluid metabolites.

Metabolomics has been attracting attention in recent years as an objective method for diagnosing schizophrenia. In this study, we analyzed 378 metabolites in the serum of schizophrenia patients using capillary electrophoresis‐ and liquid chromatography‐time‐of‐flight mass spectrometry. Using multivariate analysis with the orthogonal partial least squares method, we observed significantly higher levels of alanine, glutamate, lactic acid, ornithine, and serine and significantly lower levels of urea, in patients with chronic schizophrenia compared to healthy controls. Additionally, levels of fatty acids (15:0), (17:0), and (19:1), cis‐11‐eicosenoic acid, and thyroxine were significantly higher in patients with acute psychosis than in those in remission. Moreover, we conducted a systematic review of comprehensive metabolomics studies on schizophrenia over the last 20 years and observed consistent trends of increase in some metabolites such as glutamate and glucose, and decrease in citrate in schizophrenia patients across several studies. Hence, we provide substantial evidence for metabolic biomarkers in schizophrenia patients through our metabolomics study.

Lep gene and leptin concentration in serum of schizophrenia patients with metabolic syndrome

IntroductionSchizophrenia is associated with lower life expectancy due to cardiovascular disease. Metabolic syndrome (MetS) occupies an important place among the main problems. Indicators of hormones regulating metabolism may be appealing candidates as biomarkers of metabolic side-effects. Certain role belongs to genetic factors that might be the basis of sensitivity to development of MetS.ObjectivesThe aim is to study polymorphisms of leptin gene (LEP) and serum leptin concentration in schizophrenia patients with metabolic syndrome.MethodsAfter obtaining informed consent, patients with schizophrenia (ICD-10: F20) were included: 91 patients for biochemical research and 463 patients for genotyping. Patients were divided into two groups: 46 (119) with MetS; 45 (344) without it. Concentration of leptin was measured on an analyzer MAGPIX (Luminex, USA). Determination of 4 polymorphisms (rs2167270, rs3828942, rs10954173, rs4731426) of LEP was performed by PCR. Differences were considered significant at p&lt;0.05.ResultsThe leptin concentration is significantly (p&lt;0.001) higher in MetS (13511.5 [7392.5; 28278.75] pg/ml) compared to patients without MetS (6662 [2131.5; 11380] pg/ml). Significant differences were found in the distribution of rs3828942 (GG:GA:AA): 25.9%:44%:30.2% in MetS and 31.2%:52.6%:16.2% without MetS (χ2=10.545, p=0.005). The genotype AA and the allele A have a predisposing effect on the development of MetS (OR1=2.247, C.I:1.248-4.046; OR2=1.475, C.I:1.093-1.991, χ2=6.49, p=0.01).ConclusionsA number of features are observed in patients with MetS, which impair the functioning of patients. These investigations should aim to optimize the approach to assess the risk of MetS. The study was supported by grants from the RSF 19-75-10012 (genetic research) and 18-15-00011 (determination of leptin concentration)DisclosureThe study was supported by grants from the Russian Science Foundation №19-75-10012 (genetic research) and №18-15-00011 (determination of leptin concentration)

Determining the IgM and IgG antibodies titer against HSV1, HSV2 and CMV in the serum of schizophrenia patients.

Schizophrenia is a destructive clinical syndrome with diverse mental pathologies. Different mechanisms and factors have a role in this disease. A possible mechanism is that teratogenic viruses cause brain changes and results in the disease appearance. The schizophrenia patients were diagnosed by psychologists and with the consent of patients, five CC of venous blood was drawn. Than Serum samples were isolated and immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies against herpes simplex virus-1 (HSV-1), herpes simplex virus-2 (HSV-2) and cytomegalovirus (CMV) were quantified by ELISA sandwich kit. The Results showed that anti-CMV and anti-HSV1 and anti-HSV2 IgG antibodies in schizophrenia patients were increased significantly (p< 0.05). The increasing of the anti-HSV2 IgM was also observed but increasing amount of the anti-HSV1 IgM was not statistically significant (p< 0.05). Therefore, as a result of this study CMV and HSV1 and HSV2 infection can probably intensify the symptoms in schizophrenia patients.

Folic acid, vitamin B12 and homocysteine levels following olanzapine administration in schizophrenia patients

&lt;p class="Abstract"&gt;The purpose of this study was to assess the levels of folic acid, vitamin B&lt;sub&gt;12&lt;/sub&gt; and homocysteine in the serum of schizophrenia patients (n=20) and to evaluate the effect of olanzapine on these biomarkers. The blood was also collected from the 10 healthy volunteers as control. Compared to control, the serum folic acid (p=0.005) and vitamin B&lt;sub&gt;12&lt;/sub&gt; levels (p=0.211) were higher in the schizophrenia patients, whereas no difference was evident in the serum homocysteine level. But significantly higher levels of serum folic acid (p=0.005), vitamin B&lt;sub&gt;12&lt;/sub&gt; (p=0.047) and significantly lower level of serum homocysteine (p=0.000) were observed after 10 weeks of olanzapine administration. BPRS score was reduced significantly after intervention. The Pearson correlation coefficient test showed a statistically not significant negative relationship between the serum folate, vitamin B&lt;sub&gt;12&lt;/sub&gt; and homocysteine levels. In conclusion, olanzapine can significantly elevate the serum folic acid and vitamin B&lt;sub&gt;12&lt;/sub&gt; levels whereas it can lower the serum homocysteine level which may contribute to the improvement of symptoms of schizophrenia.&lt;/p&gt;

Increased interleukin-2 serum levels were associated with psychopathological symptoms and cognitive deficits in treatment-resistant schizophrenia

Accumulating evidence showed that interleukin-2 (IL-2) may be involved in the pathophysiology of schizophrenia. Increased IL-2 levels have been found in the serum of schizophrenia patients with mixed results. In the present study, we assessed serum IL-2 levels in a large group of 160 schizophrenia patients compared to 60 healthy control subjects matched for age and gender. The schizophrenia symptomatology was assessed by the Positive and Negative Syndrome Scale (PANSS), and serum IL-2 levels were measured by sandwich ELISA. The results showed that IL-2 levels were significantly higher in chronic patients with schizophrenia than in healthy control subjects (p<0.001). Correlation analysis revealed a significantly negative association between IL-2 levels and the PANSS cognitive and positive subscales (both p<0.01). Stepwise multiple regression analyses confirmed IL-2 as the influencing factor for the cognitive and positive subscales of the PANSS. Our findings suggested that increased IL-2 may be involved in the cognitive impairments and psychopathology of chronic schizophrenia.

Endocannabinoids and Schizophrenia

The endocannabinoids anandamide and 2-arachydonoylglycerol (2-AG) are lipids naturally derived from membrane precursors which bind cannabinoid receptors (CB1, CB2). This endocannabinoid system is disturbed in schizophrenia. Indeed, there seems to be an association between schizophrenia and polymorphisms of the CB1 receptor gene. Moreover, CB1 receptors are found in higher density in the prefrontal cortex, hippocampus and basal ganglia of patients with schizophrenia. Similarly, anandamide levels are increased in the cerebrospinal fluid (CSF) and in the serum of schizophrenia patients, including during the prodromal state, suggesting that they may play a protective role in psychosis homeostasis. Future studies are needed to further explore the role of the endocannabinoid system in the pathophysiology of schizophrenia.

Elevated plasma level of apolipoprotein D in schizophrenia and its treatment and outcome

Recently, apolipoprotein D (apoD), a protein that is involved in the essential polyunsaturated fatty acid (EPUFA) transport and metabolism, and neuronal growth and regeneration was reported to have increased in the postmortem brain and decreased in the serum of schizophrenia patients. We studied the plasma apoD levels in never-medicated schizophrenic patients at the onset of psychosis and in chronic patients with clozapine treatment. Plasma apoD levels were elevated in never-medicated patients at the first-episode of psychosis compared to normals ( P=0.047). Interestingly, the increase in apoD level was even more significant in chronic patients treated with clozapine compared to normals and first-episode patients ( P=0.008 and P=0.03, respectively). The increased apoD level in never-medicated first-episode patients indicate that this increase probably predates the illness, since the duration of illness was <5 days. Similarly, an even larger increase in apoD after clozapine treatment may be associated with its prophylactic effects, since the psychopathological scores were significantly reduced and the clozapine treatment has been found to increase the EPUFA membrane levels. These altered levels of apoD may help to understand the nature and possible mechanism of phospholipid membrane pathology in schizophrenia.