View clinical trials related to Schizophrenia.
Filter by:Wide ranging cognitive deficits are major drivers of functional decline and poor outcomes in people with schizophrenia (SZ) and bipolar disorder (BD). Medications do not target pathophysiological mechanisms thought to underlie these deficits. In the search for interventions targeting underlying cognitive impairment in SZ and BD, we look comprehensively beyond just the brain and to the potential role of dysfunctional systemic metabolism. Disrupted insulin and glucose metabolism are seen in medication-naïve first-episode SZ, suggesting that SZ itself, and not just the medications used to treat it, is associated with risk of Type 2 diabetes, cardiovascular morbidity and mortality, and more generally, accelerated aging. Even young people with SZ have increased risk of metabolic disease and cognitive deficits. Sadly, their life span is shortened by 15-20 years. BD is associated with similar but less severe disruptions in glucose and insulin metabolism and life expectancy. Although the human brain is 2% of the body's volume, it consumes over 20% of its energy, and accordingly, the brain is particularly vulnerable to the dysregulation of glucose metabolism seen in SZ and BD. While glucose is considered to be the brain's default fuel, ketones provide 27% more free energy and are a major source of energy for the brain. Ketones prevent or improve various age-associated diseases, and a ketogenic diet (70% fat, 20% protein, 10% carbohydrates) has been posited as an anti-aging and dementia antidote. The premise of the work is based on recent evidence that ketogenic diets improve dynamic neural network instability, related to cognitive deficits, aging, and Type 2 diabetes (Mujica-Parodi et al., Proc Natl Acad Sci U S A. 2020;117(11):6170-7.). The rigor of the work rests on findings of (1) poor cerebral glucose homeostasis in SZ and BD, (2) neural network instability in SZ and BD, and (3) direct effects of ketosis on network instability. Unknown is whether ketogenic diets can improve network instability in people with SZ and BD.
Schizophrenia is a heritable complex phenotype whose symptoms can be clustered into three domains: positive symptoms, negative symptoms and cognitive impairments. Constellations of negative symptoms in SCZ are composed of diminished motivation and pleasure, such as asociality, anhedonia, and avolition, or diminished expressivity such as blunted affect and alogia. Negative symptoms are associated with decreased quality of life and poor functional outcomes. Although antipsychotics are generally effective on positive symptoms, they are poorly effective on negative symptoms Currently, there are no licensed targeted medications for negative symptoms. In view of these problems, considerable interest in identifying new treatment targets for negative symptoms has grown over the past decade. Despite intense efforts in brain imaging that have opened new opportunities for addressing these issues, the neurobiological mechanism of negative symptoms remains unclear. Structural brain measures from magnetic resonance imaging (MRI) are highly heritable and representatively have high reproducibility and low measurement error. Prior neuroimaging researches have consistently shown neuroanatomical abnormalities in the brains of individuals with SCZ, with the most robust and consistent group-level structural differences in widespread reduced volumes of hippocampal thalamus, amygdala and nucleus accumbens. SCZ have been associated with widespread structural brain abnormalities, but results from neuroimaging studies have been inconsistent.
Definition: Schizophrenia is a chronic mental disorder that causes drastic changes in life quality and life functions, characterized by behavioural, cognitive and affective state deterioration. Therefore, it is regarded as one of the most important health problems causing both personal and economic problems around the world. Unhealthy lifestyle behaviours in individuals with chronic mental disorders, like schizophrenia, are emphasized to play a big part in physical health problems. For individuals to develop a healthy lifestyle behaviour, it is necessary to primarily determine the lifestyle behaviours and then prevent the illnesses caused by the lifestyle and deaths linked to these illnesses. Current theory or models used to benefit from health programmes, prepared for the development of healthy lifestyle behaviours, should be deep-scaled. Theories and models are guides for systematic planning and decision-making. A well-defined model could contribute to the process of effective health improvement programmes for directive and content creation. One of the models mainly used to develop a behavioural change in health and explain how to obtain the most effective health behavioural change is the "Transtheoretical Model". Objective: The study was conducted with the pretest-posttest randomized controlled trial design to detect the effect of psychoeducation on a healthy lifestyle, based on the Transtheoretical Model in an individual with schizophrenia. The Hypotheses of the Study Hypothesis 1: When the individuals with schizophrenia who received psychoeducation based on the Transtheoretical Model are compared to the ones that did not, they will show progress in behavioural change steps. Hypothesis 2: When the individuals with schizophrenia who received psychoeducation based on the Transtheoretical Model are compared to the ones that did not, they will have higher final test results in the healthy lifestyle scale. Methods: The data were collected from 82 participants, as 41 intervention and 41 control. The data were collected via personal information form, behavioural change stage diagnosis form and healthy lifestyle scale II. 6-week psychoeducation, consisting of 6 modules, based on the Transtheoretical model, was applied to the intervention group. No interventions were applied to the control group. Pretests and posttests were applied to both groups.
This pilot study aims to investigate the use of MRI-guided low-intensity focused ultrasound (LIFU) to modulate neuronal activity within the thalamus in human subjects with treatment-resistant schizophrenia.
We investigated the effects of Ginkgo biloba extract on the symptoms and cognitive functioning in patients with schizophrenia
Schizophrenia is a progressive psychiatric disorder with a lifetime prevalence of 1%, its etiology is not fully understood, and it progresses with relapses. There are significant differences between patients in the age of onset, frequency of attacks, response to treatment, and clinical course of the disease. Failure to respond adequately to treatment is defined as resistance to treatment and poses a great challenge in the clinical management of the disease, but the exact cause of treatment resistance has not been clarified yet. Neurodevelopmental hypothesis, neurodegenerative hypothesis, stress-diathesis hypothesis are some of them. In the neurodegenerative hypothesis, it is thought that biochemical changes cause chronic and progressive disorders of the nervous system, and schizophrenia is considered as one of these disorders. S100B, one of the biomarkers released from the central nervous system, is a glycoprotein synthesized by astrocytes; At low concentration, it ensures neuron survival, while at high concentration it causes neuronal cell apoptosis and is associated with neurodegeneration. GFAP on the other hand, can be measured in serum in proportion to the degree of damage by passing into the bloodstream as a result of astrocyte damage. It has been shown that these markers are associated with neurodegenerative diseases, autoimmune diseases and cerebrovascular pathologies and can be measured at a significant level in the blood. As far as is known, neurodegeneration has been found in patients with schizophrenia; however, there are not enough studies in the literature regarding the relationship of this neurodegeneration with treatment response and resistance. In recent years, many biomarker studies related to schizophrenia have been conducted. These studies continue in many different areas such as the early diagnosis of schizophrenia, the treatments to be applied after diagnosis, the response to the treatment given, and the clinical course of the disease, but no biomarker indicating the desired results has yet been found. In this study, measurement of s100B and GFAP serum levels in patients with treatment-resistant schizophrenia, remission schizophrenia and healthy controls, and evaluation of their relationship with response to treatment; Thus, it is aimed to investigate these points that have not been fully elucidated in the pathogenesis of schizophrenia and their use as biomarkers in predicting the response to treatment.
This pilot feasibility trial aims to evaluate the "Goals in Focus" intervention for motivational negative symptoms in people with psychosis. Goals in Focus interventions translate findings of basic clinical research on psychological mechanisms of motivational negative symptoms into a tailored and comprehensive novel psychological treatment program. The current single-blind randomized-controlled study aims to test feasibility and to examine first estimates of the expected effect size of Goals in Focus to inform a subsequent fully-powered RCT. The feasibility data will be used to improve on the trial design and the provision of the "Goals in Focus" intervention where necessary.
In previous studies the neuropeptide oxytocin has been in particular associated with social enhancing and anxiety relieving effects. The purpose of this study is to investigate the effect of oxytocin on empathy in patients with schizophrenia. On a neurobiological level, social effects mediated by oxytocin are based on oxytocin's influence on the complexly regulated mesocorticolimbic dopamine system. Preliminary studies have already shown that oxytocin increases neuronal connections between social reward expectancy networks and networks for socioemotional processes in the brain, which on a behavioral level leads to increased social activation, motivation, and also improved social perception. Furthermore, an increase in empathy modulated by the amygdala has been shown in healthy individuals following oxytocin administration. In particular, primary psychotic disorders, such as schizophrenia, are associated with deficits in the domain of social cognition, including empathy, with the degree of negative symptoms playing an important mediating role. Another study demonstrated a significantly lower expression of empathy as well as a significantly lower oxytocin level in patients with schizophrenia compared to healthy subjects. According to the hypothesis of social salience, which describes an increased importance of certain social stimuli, the effect of oxytocin varies depending on specific contexts and individual variables of the perceiving person, such as the degree of negative symptoms. Therefore, based on such preliminary findings, the research project will explore an effect of oxytocin on empathy within a positively experienced and controlled context, especially in patients with schizophrenia regarding their negative symptoms.
The purpose of this trial is to characterize the effects of 2 oral doses (over 8 weeks total) of CVL-231 on ambulatory blood pressure and heart rate in patients with stable schizophrenia.
This study aims to investigate the potential beneficial effects of a medication review by a clinical pharmacologist on patients with coexisting schizophrenia and diabetes. The study is an intervention study in which an intervention group is assigned to the medication review whereas a control group is not. Both groups are tested using a thorough test battery at baseline and 6 months after inclusion. Furthermore a qualitative data assessment will be undertaken using interviews and surveys in order to show any obstacles in implementing the intervention. This is relevant as medication reviews, performed by clinical pharmacologists as well as pharmacists, are not always implemented by the primary physician.