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Schizophrenia Group (schizophrenia + group)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Prefrontal cognition in schizophrenia and bipolar illness in relation to Val66Met polymorphism of the brain-derived neurotrophic factor gene

PSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 1 2006
JANUSZ K. RYBAKOWSKI md
Abstract, The measures of prefrontal cognition have been used as endophenotype in molecular-genetic studies. Brain-derived neurotrophic factor (BDNF) has been implicated in cognitive functions and in the pathogenesis of major psychoses. This study investigates the relationship between Val66Met polymorphisms of the BDNF gene and prefrontal cognitive function in 129 patients with schizophrenia and 111 patients with bipolar mood disorder. Cognitive tests included the Wisconsin Card Sorting Test (WCST), with such domains as number of perseverative errors, non-perseverative errors, completed corrected categories, conceptual level responses, and set to the first category, and the N-back test, where mean reaction time and percent of correct reactions were measured. Genotyping for Val66Met BDNF polymorphism was done by polymerase chain reaction method. In schizophrenia, no relationship between Val66Met polymorphism of the BDNF gene and the results of the WCST was observed. Patients with Val/Val genotype had a higher percentage of correct reactions in the N-back test than those with the remaining genotypes. Bipolar patients with Val/Val genotype obtained significantly better results on three of five domains of the WCST. No relationship between BDNF polymorphism and the results of the N-back test was found in this group. A limitation to the results could be variable psychopathological state and medication during cognitive testing and lack of Hardy,Weinberg equilibrium in schizophrenia group. Val66Met polymorphism of the BDNF gene may be associated with cognitive performance on the WCST in bipolar mood disorder but not in schizophrenia. An association of this polymorphism with performance on the N-back test in schizophrenia and not in bipolar illness may suggest that in schizophrenia, the BDNF system may be connected with early phases of information processing. [source]

Neural correlates of deficient response inhibition in mentally disordered violent individuals

BEHAVIORAL SCIENCES & THE LAW, Issue 1 2008
Ian Barkataki Ph.D.
In this study, response inhibition and associated neural activation during a motor inhibition paradigm were investigated in (i) men with antisocial personality disorder (APD) with a history of violence (n,=,14), (ii) men with schizophrenia with a history of violence (n,=,12), (iii) men with schizophrenia without a history of violence (n,=,12), and (iv) healthy control subjects (n,=,14) using functional magnetic resonance imaging (fMRI). At the behavioural level, individuals with schizophrenia showed impaired performance across all conditions, whereas an increased error rate was seen in the APD group only during the conditions requiring inhibition. At the neural level, both violent groups showed reduced thalamic activity, compared with controls, in association with modulation of inhibition by task demands. In addition, the violent schizophrenia group, compared with controls, showed reduced activity in the caudate nucleus during the condition requiring inhibition. It is concluded that violence may not be specifically associated with impaired voluntary inhibition in schizophrenia but this is likely in APD. Reduced thalamic function, perhaps due to its known association with sensorimotor disturbances, is implicated in violent behaviour across both disorders. In addition, caudate dysfunction may contribute, given its role in timing and temporal processing as well as suppression of motor actions, to deficient inhibition and violent behaviour in schizophrenia. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Effect of TGF- ,1 polymorphism on the susceptibility to schizophrenia and treatment response to atypical antipsychotic agent

ACTA NEUROPSYCHIATRICA, Issue 4 2010
Hwa-Young Lee
Lee H-Y, Kim Y-K. Effect of TGF- ,1 polymorphism on the susceptibility to schizophrenia and treatment response to atypical antipsychotic agent. Objective: Several studies have suggested that cytokine alterations could be related to the pathophysiology of schizophrenia. Transforming growth factor-beta1 (TGF- ,1) is believed to be an important factor in regulation of inflammatory responses and to have anti-inflammatory effects. TGF- ,1 also has trophic effects on dopaminergic neurons. We tested the hypothesis TGF- ,1 is associated with the pathophysiology of schizophrenia. Methods: The polymorphisms at codon 10 (T869C) and codon 25 (G915C) of TGF- ,1 were analysed in 99 schizophrenia patients and 130 normal controls. At baseline and after 8 weeks of treatment, clinical symptoms were evaluated on Positive and Negative Syndrome Scale (PANSS). Results: None of the subjects were polymorphic at codon 25. However, the C allele at codon 10 was more frequent in schizophrenia (p = 0.05). Although schizophrenia group showed a higher tendency of allele frequency in the subjects with C allele (p = 0.05), the allelic difference did not reach statistical significance after correction for multiple comparisons (p = 0.1). PANSS scores showed no significant correlation with genotypes. The genotype distribution was not significantly different between responders and non-responders. However, the C allele was more frequent among responders (p = 0.03). Conclusion: These results suggest that the TGF- ,1 polymorphism is associated with therapeutic response to antipsychotics. However, further studies with larger numbers of subjects are needed to confirm the effect of TGF- ,1 in schizophrenia. [source]

Event-related potentials and white matter lesions in bipolar disorder

ACTA NEUROPSYCHIATRICA, Issue 1 2002
E. F. P. M. Vuurman
Objectives: To investigate neurophysiological parameters which possibly distinguish subtypes I and II of patients with a bipolar disorder, and contrast the findings with observations from a group of schizophrenic patients and a group of healthy controls. Methods: Sixty-six volunteers underwent a MRI scan to determine the number and location of white matter lesions (WSL). A electrophysiological registration was made while all volunteers performed a auditory ,oddball' task, and the amplitude of the resulting P300 wave was compared. Results: Earlier reports of higher numbers of WSL in bipolar disorder were not replicated in this study. Subtypes I and II showed a different P300 amplitude and subtype I resembled the results of the schizophrenia group. Conclusion: Bipolar patients in remission have a functional brain disorder that is expressed by a change in physiological response to external stimuli. [source]