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Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects
P.3.b. Psychotic disorders and treatment − Psychotic disorders (clinical) to healthy controls. The latency of each ERPs component did not differ among groups. N100 amplitude correlated with both anhedonia and avolition domains, no correlation between P3b amplitude and the negative symptom domains was observed. Conclusions: Our results are in line with previous findings from our group indicating an association between negative symptoms and N100 amplitude reduction [5]. Avolition and Anhedonia, often clustering in the same factor, are related to abnormalities of early components of the ERPs, indexing automatic attention and perceptual processes. None of the negative symptom domains is associated with abnormalities of the later stages indexed by P3b amplitude. References [1] Millan, M.J., Fone, K., Steckler, T., Horan, W.P., 2014. Negative symptoms of schizophrenia: clinical characteristics, pathophysiological substrates, experimental models and prospects for improved treatment. Eur Neuropsychopharmacol. 24, 645−92. [2] Fulford, D., Niendam, T.A., Floyd, E.G., Carter, C.S., Mathalon, D.H., Vinogradov, S., Stuart, B.K., Loewy, R.L., 2013. Symptom dimensions and functional impairment in early psychosis: more to the story than just negative symptoms. Schizophr Res. 147, 125−31. [3] Galderisi, S., Bucci, P., Mucci, A., Kirkpatrick, B., Pini, S., Rossi, A., Vita, A., Maj, M., 2013. Categorical and dimensional approaches to negative symptoms of schizophrenia: focus on long-term stability and functional outcome. Schizophr Res. 147, 157−62. [4] Kirkpatrick, B., Strauss, G.P., Nguyen, L., Fischer, B.A., Daniel, D.G., Cienfuegos, A., Marder, S.R., 2011. The brief negative symptom scale: psychometric properties. Schizophr Bull. 37, 300−5. [5] Mucci, A., Galderisi, S., Kirkpatrick, B., Bucci, P., Volpe, U., Merlotti, E., Centanaro, F., Catapano, F., Maj, M. 2007. Double dissociation of N1 and P3 abnormalities in deficit and nondeficit schizophrenia. Schizophr Res. 92, 252−61.
P.3.b.021 Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects U. Ozkal1 ° , G. Gultekin1 , S. Incir2 , M. Emul1 , N. Konuk1 University Cerrahpasa Faculty of Medicine, Department of Psychiatry, Istanbul, Turkey; 2 Koc University, Department of Biochemistry, Istanbul, Turkey 1 Istanbul
Background: Schizophrenia is associated with the activation of immune-inflammatory pathways including the increased cytokine and chemokine levels. Recent studies of schizophrenia have been aimed to find biomarkers with a high predictive value in determining diagnosis, disease severity and treatment resistance. But few studies were made to determine the predictive abilities of these parameters. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF super family that controls many cellular activities including proliferation, migration, differentiation, apoptosis, and inflammation by binding to fibroblast growth factor-inducible 14 (Fn14), a highly inducible cell surface receptor. Elevated levels of TWEAK have been found to be associated with neuroinflammation and neurodegeneration [1,2]. Studies about TWEAK can contribute to the understanding of immune-related cytokine hypothesis of schizophrenia. The aim of this study is to investigate whether patients with schizophrenia have different serum levels of TWEAK, to compare patients with schizophrenia and healthy controls in terms of serum TWEAK levels. Methods: For this purpose, 78 patients diagnosed with schizophrenia and 42 healthy controls were compared. Patients were
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diagnosed with DSM-IV-TR diagnosis of the Structured Clinical Interview for Axis (SCID-I). Positive and Negative Syndrome Scale (PANSS) and the Brief Psychiatric Rating Scale (BPRS) were evaluated. BMI, waist circumference, systolic/diastolic blood pressure measurements have been made. Serums were stored in the freezer at −80ºC and then these blood were analyzed biochemically (C-reactive protein (CRP), fasting blood glucose, insulin, hemoglobin A1c (HbA1c), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol, triglyceride). TWEAK levels were measured by using Human TWEAK Instant ELISA kit (eBioscience, lot no: BMS2006INST). Results: There were no significant differences between patients and controls according to age, gender, body mass index and smoking (for each, p > 0.05). Serum TWEAK levels were significantly higher in patients with schizophrenia compared to control group (394.81±81.215 pg/ml, and 344.59±87.252 pg/ml, p = 0.002). Serum CRP levels were higher in patients with schizophrenia than control groups (6.91±10.29 and 2.94±2.63, p = 0.025). There were no significant correlation between serum TWEAK levels and chlorpromazine equivalent doses (p > 0.05). There were significant correlation between CRP and PANSS total score (r = 0.379 and p = 0.000) although no significant correlation between TWEAK levels, PANSS total score and smoking was observed (for each, p > 0.05). Conclusion: In line with our hypothesis, serum TWEAK and CRP levels were found higher in patients with schizophrenia than controls. There were significant correlation between CRP and PANSS scores although no correlation between TWEAK and PANSS were recorded; we considered that CRP might be a state and TWEAK might be a trade marker for schizophrenia. Prospective studies are needed to examine the relationship between inflammation, as reflected by elevated serum levels of TWEAK and treatment response as well as the moderating role of specific antipsychotic medications in patients with schizophrenia. References [1] Iocca, H.A., Plant, S.R., Wang, Y., Runkel, L., O’Connor, B.P., Lundsmith, E.T., Hahm, K., van Deventer, H.W., Burkly, L.C., Ting, J.P., 2008. TNF superfamily member TWEAK exacerbates inflammation and demyelination in the cuprizone-induced model. J Neuroimmunol 194(1−2), 97–106. [2] Potrovita, I., Zhang, W., Burkly, L., Hahm, K., Lincecum, J., Wang, M.Z., Maurer, M.H., Rossner, M., Schneider, A., Schwaninger, M., 2004. Tumor necrosis factor-like weak inducer of apoptosis-induced neurodegeneration. J Neurosci 24(38), 8237–8244.
P.3.b.022 Does community-based psychiatry approach have an effect on relapses, hospitalisations and functionality in patients with psychotic disorders? U. Ozer Ceri1 ° , C. Varlik1 , D. Sarikaya Varlik2 , O. Ozberk1 , M. Arslan Delice1 1 Bakirkoy Mazhar Osman Training and Research Hospital for Psychiatry- Neurology a, Psychiatry, Istanbul, Turkey; 2 Kackar State Hospital, Psychiatry, Rize, Turkey Background: In connection with the National Mental Health Policy published in 2006, the Ministry of Health of Turkey began to put more focus on community-based mental health services. Accordingly, starting from 2009, Community Mental Health Centers (CMHC) have been established in many regions
P.3.b.021 Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects U. Ozkal1 ° , G. Gultekin1 , S. Incir2 , M. Emul1 , N. Konuk1 University Cerrahpasa Faculty of Medicine, Department of Psychiatry, Istanbul, Turkey; 2 Koc University, Department of Biochemistry, Istanbul, Turkey 1 Istanbul
Background: Schizophrenia is associated with the activation of immune-inflammatory pathways including the increased cytokine and chemokine levels. Recent studies of schizophrenia have been aimed to find biomarkers with a high predictive value in determining diagnosis, disease severity and treatment resistance. But few studies were made to determine the predictive abilities of these parameters. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF super family that controls many cellular activities including proliferation, migration, differentiation, apoptosis, and inflammation by binding to fibroblast growth factor-inducible 14 (Fn14), a highly inducible cell surface receptor. Elevated levels of TWEAK have been found to be associated with neuroinflammation and neurodegeneration [1,2]. Studies about TWEAK can contribute to the understanding of immune-related cytokine hypothesis of schizophrenia. The aim of this study is to investigate whether patients with schizophrenia have different serum levels of TWEAK, to compare patients with schizophrenia and healthy controls in terms of serum TWEAK levels. Methods: For this purpose, 78 patients diagnosed with schizophrenia and 42 healthy controls were compared. Patients were
S507
diagnosed with DSM-IV-TR diagnosis of the Structured Clinical Interview for Axis (SCID-I). Positive and Negative Syndrome Scale (PANSS) and the Brief Psychiatric Rating Scale (BPRS) were evaluated. BMI, waist circumference, systolic/diastolic blood pressure measurements have been made. Serums were stored in the freezer at −80ºC and then these blood were analyzed biochemically (C-reactive protein (CRP), fasting blood glucose, insulin, hemoglobin A1c (HbA1c), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol, triglyceride). TWEAK levels were measured by using Human TWEAK Instant ELISA kit (eBioscience, lot no: BMS2006INST). Results: There were no significant differences between patients and controls according to age, gender, body mass index and smoking (for each, p > 0.05). Serum TWEAK levels were significantly higher in patients with schizophrenia compared to control group (394.81±81.215 pg/ml, and 344.59±87.252 pg/ml, p = 0.002). Serum CRP levels were higher in patients with schizophrenia than control groups (6.91±10.29 and 2.94±2.63, p = 0.025). There were no significant correlation between serum TWEAK levels and chlorpromazine equivalent doses (p > 0.05). There were significant correlation between CRP and PANSS total score (r = 0.379 and p = 0.000) although no significant correlation between TWEAK levels, PANSS total score and smoking was observed (for each, p > 0.05). Conclusion: In line with our hypothesis, serum TWEAK and CRP levels were found higher in patients with schizophrenia than controls. There were significant correlation between CRP and PANSS scores although no correlation between TWEAK and PANSS were recorded; we considered that CRP might be a state and TWEAK might be a trade marker for schizophrenia. Prospective studies are needed to examine the relationship between inflammation, as reflected by elevated serum levels of TWEAK and treatment response as well as the moderating role of specific antipsychotic medications in patients with schizophrenia. References [1] Iocca, H.A., Plant, S.R., Wang, Y., Runkel, L., O’Connor, B.P., Lundsmith, E.T., Hahm, K., van Deventer, H.W., Burkly, L.C., Ting, J.P., 2008. TNF superfamily member TWEAK exacerbates inflammation and demyelination in the cuprizone-induced model. J Neuroimmunol 194(1−2), 97–106. [2] Potrovita, I., Zhang, W., Burkly, L., Hahm, K., Lincecum, J., Wang, M.Z., Maurer, M.H., Rossner, M., Schneider, A., Schwaninger, M., 2004. Tumor necrosis factor-like weak inducer of apoptosis-induced neurodegeneration. J Neurosci 24(38), 8237–8244.
P.3.b.022 Does community-based psychiatry approach have an effect on relapses, hospitalisations and functionality in patients with psychotic disorders? U. Ozer Ceri1 ° , C. Varlik1 , D. Sarikaya Varlik2 , O. Ozberk1 , M. Arslan Delice1 1 Bakirkoy Mazhar Osman Training and Research Hospital for Psychiatry- Neurology a, Psychiatry, Istanbul, Turkey; 2 Kackar State Hospital, Psychiatry, Rize, Turkey Background: In connection with the National Mental Health Policy published in 2006, the Ministry of Health of Turkey began to put more focus on community-based mental health services. Accordingly, starting from 2009, Community Mental Health Centers (CMHC) have been established in many regions