View clinical trials related to Schizophrenia.
Filter by:Schizophrenia is an invalidating psychiatric illness with a strong genetic component characterized by abnormal processing of emotional information. This alteration in emotion processing has been described in acute as well as in remission phases of the illness. It has also been found in healthy relatives of patients with schizophrenia and in subjects at high risk of psychosis. Thus, alterations in emotional information processing are not only linked to the prognosis but can also be considered as a marker of vulnerability of schizophrenia. In addition, schizophrenia patients differ from healthy controls in neural activity in brain regions implicated in emotions processing. However, interpretation of findings in patients is limited by confounding factors, such as antipsychotic treatments or alterations due to the course of illness. Also, there is no data concerning genetic factors (polymorphisms or gene expression) underlying these patterns of cerebral activation in emotion information processing. So, the main objective of this study is to compare the cerebral activity of schizophrenia patients to that of healthy siblings and healthy controls in an emotional processing task.
Theory of mind (TOM), a main component of social cognition processes, refers to the capacity to infer one's own and other person's mental states. Deficits in social cognition are found in patients with schizophrenia and bipolar disorder. The purpose of this study is to compare the neurofunctional profiles of schizophrenic patients, bipolar patients and healthy participants during the performance of a TOM task. Results may help to understand the neural bases of the impairments in social cognition in schizophrenia and bipolar disorder, which may in turn help to propose potential new psychosocial therapeutic approaches in these disorders.
Caffeine is the most used psychoactive drug in Canada, with regular consumption by 88% of the adult population, While rates of caffeine consumption are considered to be high in the general population, there is some evidence that they may be even higher within schizophrenia patients; in a 2006 U.S. study, daily consumption rates of caffeine were nearly double those observed in a healthy control population (471.6 mg/day vs. 254.2 mg/day). Furthermore, 13% of the schizophrenia population studied ingested more than 1000 mg/day of caffeine, well above the 400 mg daily maximum recommended by Health Canada. High doses of caffeine are particularly concerning for individuals with schizophrenia; caffeine alters dopaminergic activity at post-synaptic neurons through its actions at adenosine A2A receptors, which may exacerbate positive symptoms, such as delusions and hallucination. This significant rate of consumption is likely due in part to caffeine's actions on the human brain, resulting in increased arousal, elevated mood and beneficial effects on a wide-range of cognitive processes including verbal working memory, sustained attention, and executive function. These areas of caffeine-induced cognitive improvement notably overlap with the cognitive domains that are reported to be diminished in schizophrenia. Despite this overlap and the rates of caffeine consumption observed within schizophrenia, research reports examining the effects of caffeine on cognition and brain activity are all but non-existent in this population. The primary objective of this proposal is to compare the effects of caffeine and placebo on brain function during cognitive tasks in participants with schizophrenia. While the investigators have specific hypotheses for each task, overall the investigators hypothesize that caffeine will improve cognitive function (as evidenced by larger ERP amplitudes and/or reduced ERP latencies) compared to placebo in schizophrenia patients, with similar effects (albeit reduced in magnitude) observed in non-patient healthy controls.
The objective of the study is to investigate the efficacy, safety and pharmacokinetics of four different doses of BI 425809 once daily compared to placebo given for 12 weeks in patients with schizophrenia on stable antipsychotic treatment.
This study is intended to determine whether the addition of trospium chloride to xanomeline tartrate will ameliorate the peripheral cholinergic side effects that have been previously experienced with xanomeline tartrate when administered alone.
The investigators recently showed that visuomotor integration was significantly altered in schizophrenic patients during: (i) a grip force task (Teremetz et al., 2014), and (ii) a saccadic paradigm (oculomotor task)(Amado et al., 2008). Given this findings, the investigators propose a combined study of oculomotor and grip force control to better characterize the sensorimotor integration deficit. This approach may allow for identification of behavioural biomarkers of vulnerability to develop schizophrenia.
This study involves evaluating the occupancy of ATI-9242 at steady state at three different dose levels on D2 receptors in the brain using [18F] Fallypride PET in up to three cohorts of subjects.
This is a multicenter, randomized, double-blind, placebo-controlled, three period crossover study to evaluate the effects of RO5545965 on the functioning of key brain circuitry involved in negative symptoms using functional magnetic resonance imaging (fMRI) and reward-based learning in stable participants with mild to moderate negative symptoms of schizophrenia treated with antipsychotics. Participants will be randomized to one of six different sequences during which each participant will receive three 3-week treatment courses with RO5545965 5 milligrams (mg), RO5545965 15 mg and placebo. Each treatment period will be separated by a washout period of 14 days. Total duration of study will be approximately 17 weeks.
Impairments of cognition are a core, severely disabling feature of schizophrenia leading to poor long-term outcome with no established treatment available. Particularly impaired executive functions (e.g working memory) are frequently observed and are consistently associated with reduced activation of the dorsolateral prefrontal cortex (dlPFC). Deficits in those functions have been shown to be closely related to negative symptoms, thought disorder, and functional outcome in schizophrenia leading to the notion that frontal lobe dysfunction is crucially important in schizophrenic psychopathology. Noninvasive brain stimulation like tDCS can enhance executive functions like working memory in healthy subjects as well as in patients. To identify the optimal parameters for this intervention in patients with schizophrenia, the investigators first test the effects of different polarities (anodal, cathodal), stimulation intensities (1mA, 2mA) and laterality (left, right) on working-memory performance (nback task) in a sham-controlled cross-over design (n=128). To elucidate mechanisms of action, oscillatory brain activity will be registered with electroencephalography (EEG). These experiments will provide reliable data for an evidence-based development of new clinical interventions to improve treatment of cognitive deficits in patients with schizophrenia and thus enhance schizophrenia prevention and recovery.
This is a confirmatory randomized controlled trial of the efficacy of a novel intervention combining neuroplasticity-based cognitive training with aerobic exercise, compared to the same systematic cognitive training alone. Treatment occurs for 6 months after randomization, with a followup assessment at 12 months. The investigators hypothesize that combining neuroplasticity-based computerized cognitive training and neurotrophin-enhancing physical exercise will produce neurotrophin increases and cognitive and functional improvements, even relative to cognitive training alone. The investigators target the period shortly after a first episode of schizophrenia to maximize the generalization of cognitive improvement to functional outcome, before chronic disability is established.