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Schizophrenia Subtype (schizophrenia + subtype)
Selected AbstractsNegative symptoms of schizophrenia: a problem that will not go awayACTA PSYCHIATRICA SCANDINAVICA, Issue 1 2007S. M. Stahl Objective:, Negative symptoms of schizophrenia are a common, enduring, and debilitating component of the psychopathology of schizophrenia. Although efforts thus far to elucidate a distinct schizophrenia subtype based upon negative symptoms have yielded mixed results, there are nevertheless neurobiological correlates of the negative symptom typology. Method:, A review of nosology, typology, and assessment tools for determining core negative symptoms in schizophrenia. Results:, Negative symptoms can be difficult to evaluate objectively. Current rating scales ,capture' key domains of negative symptoms, in spite of considerable overlap between these domains. However, each objective assessment trades off methodological rigor and detail against brevity of assessment and ease of use. Conclusion:, The description of new methods for measuring these devastating symptoms, coupled with the ongoing development of novel antipsychotics and agents that augment antipsychotics have fuelled renewed interest in the evaluation of negative symptoms and optimism that better treatments for negative symptoms can be found. [source] Association study of a promoter polymorphism of UFD1L gene with schizophreniaAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 6 2001Alessandro De Luca Abstract Schizophrenia or schizoaffective disorders are often found in patients affected by DiGeorge/velo-cardio-facial syndrome (DGS/VCFS) as a result of hemizygosity of chromosome 22q11.2. We evaluated the UFD1L gene, mapping within the DGS/VCFS region, as a potential candidate for schizophrenia susceptibility. UFD1L encodes for the ubiquitin fusion degradation 1 protein, which is expressed in the medial telencephalon during mouse development. Using case control, simplex families (trios), and functional studies, we provided evidence for association between schizophrenia and a single nucleotide functional polymorphism, ,277A/G, located within the noncoding region upstream the first exon of the UFD1L gene. The results are supportive of UFD1L involvement in the neurodevelopmental origin of schizophrenia and contribute in delineating etiological and pathogenetic mechanism of the schizophrenia subtype related to 22q11.2 deletion syndrome. © 2001 Wiley-Liss, Inc. [source] Total antioxidant response in patients with schizophreniaPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2006BILAL USTUNDAG md Abstract, There is a large amount of convincing data demonstrating that reactive oxygen species (ROS) are involved in initiation and development of many different forms of neuropsychiatric disorders. The levels of oxidants and antioxidants in schizophrenia have been evaluated. However, measurements of total antioxidant response (TAR) were not evaluated up to now. Therefore, the objectives of this study are to investigate plasma TAR levels in schizophrenia subtypes. A total of 76 patients with schizophrenia and 25 healthy volunteers were included in the study. Positive and Negative Syndrome Scale (SANS and SAPS, respectively) were applied to patients. TAR values were determined in the plasma of normal healthy controls and patients with schizophrenia. Plasma TAR levels of each schizophrenia subtype were significantly lower than healthy controls (P < 0.01 for disorganized, residual and undifferentiated subtypes and P < 0.01 for paranoid subtype). When intragroup comparisons were performed, paranoid subtype had higher plasma TAR levels compared to other subtypes (P < 0.01). Accordingly, as a whole group, patients with schizophrenia had lower plasma TAR levels compared to controls. Plasma TAR levels were significantly and negatively correlated with SANS scores, and duration of illness was evaluated but not related to other parameters. Consequently, the present study further emphasizes the growing consideration that free radical damage may have an important etiopathogenetic role on the development of schizophrenia and suggests that decreased plasma total antioxidant levels may be related to the progression of illness. [source] The PIP5K2A and RGS4 genes are differentially associated with deficit and non-deficit schizophreniaGENES, BRAIN AND BEHAVIOR, Issue 2 2007S. C. Bakker Several putative schizophrenia susceptibility genes have recently been reported, but it is not clear whether these genes are associated with schizophrenia in general or with specific disease subtypes. In a previous study, we found an association of the neuregulin 1 (NRG1) gene with non-deficit schizophrenia only. We now report an association study of four schizophrenia candidate genes in patients with and without deficit schizophrenia, which is characterized by severe and enduring negative symptoms. Single-nucleotide polymorphisms (SNPs) were genotyped in the DTNBP1 (dysbindin), G72/G30 and RGS4 genes, and the relatively unknown PIP5K2A gene, which is located in a region of linkage with both schizophrenia and bipolar disorder. The sample consisted of 273 Dutch schizophrenia patients, 146 of whom were diagnosed with deficit schizophrenia and 580 controls. The strongest evidence for association was found for the A-allele of SNP rs10828317 in the PIP5K2A gene, which was associated with both clinical subtypes (P = 0.0004 in the entire group; non-deficit P = 0.016, deficit P = 0.002). Interestingly, this SNP leads to a change in protein composition. In RGS4, the G-allele of the previously reported SNP RGS4-1 (single and as part of haplotypes with SNP RGS4-18) was associated with non-deficit schizophrenia (P = 0.03) but not with deficit schizophrenia (P = 0.79). SNPs in the DTNBP1 and G72/G30 genes were not significantly associated in any group. In conclusion, our data provide further evidence that specific genes may be involved in different schizophrenia subtypes and suggest that the PIP5K2A gene deserves further study as a general susceptibility gene for schizophrenia. [source] Total antioxidant response in patients with schizophreniaPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2006BILAL USTUNDAG md Abstract, There is a large amount of convincing data demonstrating that reactive oxygen species (ROS) are involved in initiation and development of many different forms of neuropsychiatric disorders. The levels of oxidants and antioxidants in schizophrenia have been evaluated. However, measurements of total antioxidant response (TAR) were not evaluated up to now. Therefore, the objectives of this study are to investigate plasma TAR levels in schizophrenia subtypes. A total of 76 patients with schizophrenia and 25 healthy volunteers were included in the study. Positive and Negative Syndrome Scale (SANS and SAPS, respectively) were applied to patients. TAR values were determined in the plasma of normal healthy controls and patients with schizophrenia. Plasma TAR levels of each schizophrenia subtype were significantly lower than healthy controls (P < 0.01 for disorganized, residual and undifferentiated subtypes and P < 0.01 for paranoid subtype). When intragroup comparisons were performed, paranoid subtype had higher plasma TAR levels compared to other subtypes (P < 0.01). Accordingly, as a whole group, patients with schizophrenia had lower plasma TAR levels compared to controls. Plasma TAR levels were significantly and negatively correlated with SANS scores, and duration of illness was evaluated but not related to other parameters. Consequently, the present study further emphasizes the growing consideration that free radical damage may have an important etiopathogenetic role on the development of schizophrenia and suggests that decreased plasma total antioxidant levels may be related to the progression of illness. [source] | |||||||||||||