Active clinical trials for "Schizophrenia"

To study the impact of genetic and environmental factors on high-level cognition associated neural circuits among healthy young Chinese Han subjects.

Learning includes the ability to generalize to new situations and respond to similar, yet not identical stimuli. In previous work, focused on stimulus generalization in healthy volunteers, tones that were negatively reinforced induce wider generalization curves than tones that were positively reinforced, and these in turn induce wider curves than neutral memory (Schechtman et al, 2010). The current study aimed to evaluate those patterns in different clinical disorders (including Schizophrenia, Bipolar disorder, MDD, Anxiety disorders (Panic and GAD) and PTSD, and healthy subjects that would be used as a control), with consideration whether those patterns are unique to any specific disorder or state. The generalization patterns evaluation would conduct twice though enable to compare the stability of those patterns during the course of the illness (i.e during remission compared to acute state). The basic paradigm based on conditioning of a tone (sound) with unpleasant noise, and extinction of that conditioning afterword. During the 60 minutes of evaluation, the capability to discriminate between the original tone and similar but not identical tones, and the tendency to categorize similar tones as identical to the original tone. A neutral tone without conditioning will be used as reference. The clinical diagnosis will conduct by a senior psychiatrist, and the state would be evaluated using standard questionnaires

The goal of this research is to understand whether schizophrenic patients are capable of comprehending clinical trial consent form or influenced by disease, also after intensified educational illustration for "understanding of consent form", their comprehension increased or not, in order to protect patient's right.

A prospective, longitudinal, multi-centre investigation (16 centres), including 562 patients, consecutively referred during two years, with a first-episode psychosis of ICD-10, F-2 type. Patients were treated with: 1) 'Supportive psychodynamic psychotherapy as a supplement to treatment as usual', 2) an 'Integrated, assertive, psychosocial and educational treatment programme', and 3) 'Treatment as usual'.

Apathy, defined as a quantitative reduction of voluntary, goal-directed behaviours (GDB), is a core component of negative symptoms. It has been suggested that the physiopathology of apathy is not a single entity but may be multiple, depending on which specific process or macrofunction is disrupted during completion of GDB. In line with this notion, Levy and Dubois proposed dividing apathic syndromes into three subtypes of disrupted processing: 'a-motivation', 'cognitive inertia', and 'uncoupling'. In schizophrenia, apathy has been associated with executive dysfunction, functional impairment and poor outcome. However, the neurobiological underpinnings of apathy in schizophrenia are poorly understood. Primary objective: confirm that chronic schizophrenic patients are apathic compared to healthy volunteers Secondary objectives: investigate if apathy is related to a particular aspect of the disease (i.e. negative, positive symptomatology and/or deficit form) investigate if apathy correlates with executive dysfunction investigate if apathy is associated with a specific mechanism using an experimental task specially designed to investigate the different mechanism (i.e. 'a-motivation', 'cognitive inertia', and 'uncoupling') investigate if there is a volumetric abnormality affecting the executive system in apathic schizophrenic patients link these eventual volumetric abnormalities to prefrontal cortex-basal ganglia circuits according to a specific subtype of apathy in the apathic schizophrenic group

Schizophrenia is a disabling mental disease affecting about 1% of the worldwide population. There is an overall heritability estimate of 68% for the underlying liability to schizophrenia. Molecular epigenetic studies can overcome the complexities of traditional genetic studies and provide a new framework for the search of etiological factors in schizophrenia. DNA methylation provides an example of an epigenetic process that affects gene expression. Several postmortem experiments have found that increased DNA methylation at the glutamic acid decarboxylase (GAD67) and reelin promoter, and hypomethylation of membrane-bound catechol-O-methyltransferase (MB-COMT) promoter gene in prefrontal cortex of schizophrenia patients. Because it is impossible to obtain brain tissue from schizophrenia patients clinically, the peripheral blood mononuclear cell (PBMC) can partly represent the brain gene expression. It has been reported to use PBMC as biomarkers for epigenetic abnormalities, such as histone acetylation and methylation, in schizophrenia. To the investigators best knowledge, gene promoter DNA methylation abnormalities in schizophrenia have been limited to postmortem study. It warrants to studying the DNA methylation using schizophrenia's PBMC. Recently, endophenotype strategy has emerged as an important tool in understanding the genetic architecture of schizophrenia. Some cognitive functions, such as attention and working memory (WM), have been used as candidate endophenotypes for genetic studies in schizophrenia. Synchronized GABA neurotransmission in the dorsolateral prefrontal cortex is required for adequate attention and working memory, suggesting that impairments in GABA-mediated inhibition in the prefrontal cortex could contribute to the endophenotype presentations in schizophrenia.

The objective of the suggested study is to identify changes in MEG correlates caused by the add-on treatment with the changes in negative symptoms of schizophrenia by comparing the change in the MEG correlates of the subjects before and during usage of new add on treatments for negative symptoms. The investigators hypothesize that the gravity of negative symptoms will correlate with a trend towards more aberrant electroencephalographic correlates mainly in continuous parameters, with an emphasis on alpha and delta bands

The goal of this research is to find out possible susceptible gene(s) in schizophrenic patients with family history and 5-year period functional changes of brain among the members of family, in order to further analysis factors and their interactions.

Schizophrenia is a severe mental illness which is considered to have, among other, a genetic etiology. One of the most efficient tools in genetic-psychiatry is the investigation of multiplex families. The current study will identify patients of multiplex families and to map their family connections and the presence of mental illnesses among family members.

Impact of stigma on the empathy and quality of life of people with schizophrenic disorders and their siblings.