Active clinical trials for "Schizophrenia"

This study's primary objective is to perform a randomized controlled pilot study to assess the feasibility of using EEG-based neurofeedback to reduce the severity of treatment-resistant auditory verbal hallucinations ('hearing voices') in patients diagnosed with schizophrenia. Patients will be randomized to receive either EEG-based neurofeedback or treatment-as-usual.

The purpose of this study is to assess the safety and tolerability of AMG 579 following a single oral dose administration in healthy subjects (Part A) and in patients with schizophrenia or stable schizoaffective disorder (Part B). The study in healthy subjects (Part A) concluded, and following a protocol amendment, enrolled only patients with schizophrenia or stable schizoaffective disorder (Part B).

The aim of the investigators project is to explore the mechanisms of pain insensitivity in patients with schizophrenia, in order to prevent its invalidating consequences. The investigators will couple methods of experimental psychology with EEG and blood samplings, in order to distinguish the role of non-painful perception, attention, aversive effects, and pain expression, and the investigators will explore an original neurobiological hypothesis regarding the activation of opioid receptors.

To compare inpatient psychiatric hospitalization rates while participants are on oral standard-of-care antipsychotic treatment and later switched to Abilify MyCite®.

The purpose of this study is to address the shortcoming in clinical hallucination research by causally manipulating the neural loci of conditioned hallucination task behavior in-person in patients with psychosis using transcranial magnetic stimulation (TMS), tracking the impact of this manipulation on the number of times participants with hallucinations report hearing tones that were not presented. With such a causal intervention, the veracity of this explanation of hallucinations will be either validated or disconfirmed. If validated, the task can be further developed as a biomarker for predicting the hallucination onset, guiding, developing or tracking the effects of treatments for hallucinations.

The purpose of this study is to determine the safety, tolerability and pharmacokinetics (PK) of single and multiple rising doses of TAK-831 in healthy participants.

Phosphodiesterase (PDE) inhibitors represent a new group of potential antipsychotic compounds currently under development. One of these is papaverine, an inhibitor of the PDE 10 family. The class of PDE10 inhibitors have been reported as possible candidates in the treatment of schizophrenia, and may prove an attractive antipsychotic alternative due to the many side-effects of the currently available antipsychotics. It has been proposed from preclinical studies that PDE10 inhibitors have the potential to reduce cognitive deficits in schizophrenia and these findings need to be confirmed in a human population, in view of the fact that no other currently registered drug posses these unique properties. The currently proposed project is designed to investigate whether the PDE10 inhibitor Papaverine indeed have the capacity to reduce cognitive deficits in schizophrenia patients. In order to accomplish this effect, Papaverine will be investigated in schizophrenia, with regards to symptomatology, hemodynamic, neurocognition and early information-processing.

The goal of this project is to understand whether glycine is helpful for improving some symptoms of schizophrenia such as low motivation, loss of interest, and social isolation. In addition, the investigators want to find out if glycine improves memory. This project involves a three-and-a-half month trial of glycine or placebo. A placebo looks exactly like the study drug, but it contains no active drug. Glycine is a naturally occurring substance that is a part of some of the proteins in your body. Glycine has not been approved by the FDA (Food and Drug Administration) for the treatment of schizophrenia. However, the FDA allows it to be used in research studies. Related Study at McLean Hospital: If you would like to participate in this study of glycine versus placebo at the Freedom Trail Clinic, the investigators will ask you if you would also like to participate in a related study at McLean Hospital. The study at McLean Hospital will look at the effects of glycine and placebo on levels of glycine in the brain. The study will use magnetic resonance spectroscopy to measure brain glycine levels. The magnetic resonance (MR) scanner looks like a large cylinder with a tube running down the center. You will be asked to lie down on your back on a foam-padded table and place your head into a special holder. The table will slide you inside the "hole" of the scanner. Soft foam rubber sponges may be placed on both sides of your head for comfort and to help keep your head from moving. Because the scanner contains a strong magnet, you will be asked to remove all metal objects from your person including, but not limited to: watches, rings, necklaces, bracelets, earrings and other body piercings, belts, loose change, wallet (with credit cards), items of clothing containing magnetic materials (for example, underwire bras, certain types of zippers), and shoes. These items will be secured in a safe place until your scan is completed. You will be able to remain in your street clothes. The investigators will ask you if study staff from McLean Hospital can contact you to tell you more about the study. You may refuse to be contacted by McLean Hospital. However, if you do not participate in the study at McLean, you are not eligible for the study here at the Freedom Trail Clinic.

Social cognition impairment is critical to the pathology and morbidity of a number of psychiatric disorders, including the schizophrenia spectrum, the autism spectrum and the personality disorders, thus representing a dimension consistent with RDoC. As such, this study aims to a) further characterize the unique deficits in social cognition (recognition and interpretation of social cues and representation of thoughts, intentions, and feelings of others) across disorders, including the schizophrenia spectrum (which includes schizophrenia, SCZ, schizoaffective disorder, SAD, bipolar disorder, BD, and schizotypal personality disorder, SPD), the autism spectrum disorders (ASD), and borderline personality disorder (BPD) compared to healthy controls (HC); b) assess the effect of intranasal oxytocin (OXT) as a regulator and novel treatment of social cognition impairment in these disorders; and c) enhance our understanding of the specificity and exact mechanisms of impairment to inform the accurate dosing of OXT required to modulate social cognition in these disorders and identify a model of optimum social cognitive function. Addressing these questions will further catalyze research into a model of optimum social cognitive activity, and accelerate industry development of agents suited to routine clinical administration.

Approximately 25% of people with schizophrenia abuse marijuana. These people may be using marijuana to self-medicate symptoms such as hallucinations (hearing or seeing things that are not heard or seen by others) or delusions (false beliefs i.e. people are harassing or persecuting them) or the depressed and anxious feelings brought on by these symptoms. Currently, it is unknown whether marijuana makes schizophrenia better or worse. Marijuana intoxication in people without schizophrenia generally causes decreased recall of words, may decrease reaction time and decrease inhibition. Additionally, marijuana may cause distractibility as demonstrated by difficulty keeping their eyes on a moving target and difficulty inhibiting their response to repetitive tones. However, marijuana may have different effects in schizophrenia. Receptors for cannabis (marijuana) are concentrated in the brain and maladjustment of the cannabinoid system may be associated with the difficulty in thinking found in schizophrenia. The proposed research project examines if clinical symptoms, learning, memory, inhibition and distractibility are improved or made worse by the acute ingestion of tetrahydrocannabinol (THC).