Introductıon:We aimed to determine the serum levels of transactive response of DNAMethods:The study group was composed of thirty children aged between 6 and 10. They were diagnosed with ADHD according to DSM-IV criteria. They were the subjects who applied to Dicle University, Faculty of Medicine, and Department of Child Psychiatry in Diyarbakır, Turkey. Children with ADHD were assessed via Turgay DSM-IV Based Child and Adolescent Behavior Disorders Screening and Rating Scale and Stroop test. Serum TDP-43 and UCH-L1 levels were analysed with enzyme-linked immunosorbent assay.Results:The TDP-43 and UCH-L1 serum levels of children with ADHD were found to be statistically significantly higher than those of controls. On the other hand, we found that serum levels of TDP-43 correlated with interference effect and hyperactivity–impulsivity in children with ADHD.Conclusıon:Imbalances in serum UCH-L1 and TDP-43 levels, and the correlation of TDP-43 levels with clinical parameters in children with ADHD may suggest that ubiquitin-proteasome pathway alterations are associated with ADHD. Deterioration of this pathway may cause intracellular TDP-43 aggregation.

α-Synuclein (α-syn) and tau proteins are thought to be related with the synaptic loss and cell death underlying several important neurodegenerative diseases. The aim of our study was to investigate serum α-syn and tau levels in autism. Serum levels of α-syn and tau were measured, and autism spectrum disorder (ASD) severity was assessed at admission using the Childhood Autism Rating Scale (CARS) total score. The mean CARS score of the autism group on admission was 47.91 points (SD: 5.97). The results indicated that the mean serum α-syn and serum tau levels were significantly (p < 0.001) lower in children with ASD as compared with normal cases (33.01 ± 20.78 and 55.19 ± 15.34 ng/mL and 241.23 ± 290.5 and 509.78 ± 269.25 ng/mL, respectively). There was a significant positive correlation between serum α-syn levels and serum levels of tau identified by Pearson correlation analysis (r = 0.922, n = 28, p < 0.001). Synaptic abnormality in autism may result from microglial activity. Furthermore, α-syn and tau aggregation may lead to synaptic dysfunction, and this may contribute to either neuronal or synaptic dysfunction or neurodegeneration. Our preliminary study suggests that low levels of serum α-syn and tau may be implicated in the relationship between synaptic activity and autism.

Objectiveα-synuclein, Nogo-A and Ubiquitin C-terminal hydrolase L1 (UCH-L1) have neuromodulatory roles for human brain. Therefore, abnormalities of these molecules are associated with neuropsychiatric disorders. Although some serum studies in the other disorders have been made, serum study of α-synuclein, Nogo-A and UCH-L1 is not present in patients with schizophrenia and healthy controls. Therefore, our aim was to compare serum levels of α-synuclein, Nogo-A and UCH-L1 of the patients with schizophrenia and healthy controls.MethodsForty-four patients with schizophrenia who is followed by psychotic disorders unit, and 40 healthy control were included in this study. Socio-demographic form and Positive and Negative Syndrome Scale (PANSS) was applied to patients, and sociodemographic form was applied to control group. Fasting bloods were collected and the serum levels of α-synuclein, Nogo-A and UCH-L1 were measured by ELISA method.ResultsSerum α-synuclein [patient: 12.73 (5.18–31.84) ng/mL; control: 41.77 (15.12–66.98) ng/mL], Nogo-A [patient: 33.58 (3.09–77.26) ng/mL; control: 286.05 (136.56–346.82) ng/mL] and UCH-L1 [patient: 5.26 (1.64–10.87) ng/mL; control: 20.48 (11.01–20.81) ng/mL] levels of the patients with schizophrenia were significianly lower than healthy controls (p<0.001).ConclusionOur study results added new evidence for explaining the etiopathogenesis of schizophrenia on the basis of neurochemical markers.

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Tau protein is located in the axons of neurons and in Alzheimer Disease, is abnormally phosphorylated and aggregates into paired helical filaments (neurofibrillary tangles) reflecting the degree of neurofibrillary pathology and neurodegeneration. Although tau and phosphorylated tau (p-Tau) pathology is a hallmark for dementia, few studies were performed in patients of schizophrenia. This preliminary serum study was designed to compare serum total tau and p-Tau levels of schizophrenia patients with healthy controls. The study was included 42 patients diagnosed with schizophrenia and 42 healthy control subjects. Sociodemographic form was applied to both groups and PANSS was applied to patient group. Serum total tau and p-Tau levels were measured by ELISA method. Total tau and p-Tau levels of patients were significantly lower than healthy controls. There was a positive correlation between amount of past electroconvulsive therapies and total tau level. However total tau and p-Tau levels were positively correlated. Our study results showed that serum total tau and p-Tau levels of patients with schizophrenia were significantly lower than healthy controls.

The effects of escitalopram treatment on oxidative/antioxidative parameters in patients with depression Objective: In this study, we aimed to investigate the effects of escitalopram, an antidepressant drug of the selective serotonin reuptake inhibitor group, on lipid peroxidation, nitric oxide (NO) level and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in patients with major depressive disorder. Method: Eighteen patients (11 women, 7 men) diagnosed with major depressive disorder (MDD) according to DSM-IV criteria and eighteen healthy controls (10 women, 8 men) were included in the study. The relevant parameters were measured before and after treatment with 20 mg/day escitalopram for 6 weeks in patients and only once in the controls. Results: Plasma SOD, CAT, malondialdehyde (MDA) and NO levels were significantly higher before treatment in patients with major depression compared to healthy controls; there was no significant differences in GPx levels. Treatment with 20 mg/day escitalopram for 6 weeks reduced plasma SOD, CAT, MDA and NO levels statistically significantly; it had no effect on GPx levels. Conclusion: The results provide evidence for the role of oxidative stress in the pathogenesis of MDD and revealed that subchronic treatment with escitalopram significantly decreased the activity of antioxidant enzymes and MDA values. It may be argued that antioxidant enzymes such as SOD, CAT and oxidative stress markers such as MDA and NO are state markers of MDD, because values came close to the results of healthy subjects after treatment.

BackgroundAlthough majority of the previous studies have shown a good correlation between enzyme linked immuno sorbent assay (ELISA) and flow cytometry in terms of cytokines, two laboratory methods usually were compared with the regression analysis and correlation in the literature. This study aimed at comparing the ELISA and flow cytometry assay for measuring cytokines by using two different statistical methods, regression analysis and Bland-Altman plot.Materials and methodsFifty patients, diagnosed with hypercholesterolemia and expecting high level serum cytokines, and 30 healthy volunteers, expecting normal level serum cytokines, were enrolled in the study. The interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured using ELISA, and compared with obtained levels using flow cytometric method.ResultsAlthough regression analysis showed that the two methods are compatible with measurements of IL-1β, IL-6 and TNF-α, they tended to show dissimilarity with measurements of IL-1β and TNF-α based on Bland-Altman graphs.ConclusionAccording to Bland-Altman plot, our results providing evidence of ELISA and flow cytometry assays were compatible with each other for IL-1β and IL-6 measurements compared to TNF-α measurement. However, our study has a small number of participants, hence this study need to be confirmed by investigations involving more participants.

It will be of great interest to determine other potential causes of elevated serum levels of GFAP, and whether this elevation has any phenotypic effect.