60 Participants Needed

Synaptic Imaging for Schizophrenia

Recruiting at 1 trial location
SC
SC
Overseen ByStudy Coordinator 2
Age: 18+
Sex: Any
Trial Phase: Phase 1
Sponsor: Davidzon, Guido, M.D.
Must be taking: Antipsychotics
No Placebo GroupAll trial participants will receive the active study treatment (no placebo)

Trial Summary

Will I have to stop taking my current medications?

The trial requires that participants with schizophrenia be on a stable medication regimen for at least two weeks before testing, so you will not need to stop taking your current medications.

What evidence supports the effectiveness of the drug [11C]UCB-J for schizophrenia?

Research shows that people with schizophrenia have lower levels of synaptic density, which is linked to the severity of symptoms. The drug [11C]UCB-J is used in imaging to detect these lower levels, helping to understand and potentially track the progression of the disease.12345

Is the [11C]UCB-J radiotracer safe for use in humans?

The [11C]UCB-J radiotracer has been used in human studies to measure synaptic density, and whole-body scans have been performed to determine its radiation dosimetry, which is a measure of the radiation dose absorbed by the body. This suggests that it has been evaluated for safety in terms of radiation exposure in humans.25678

How does the drug 11C-UCB-J differ from other treatments for schizophrenia?

The drug 11C-UCB-J is unique because it uses PET imaging to measure synaptic vesicle density in the brain, which is a novel approach for understanding and potentially diagnosing schizophrenia. Unlike traditional treatments that focus on symptom management, this drug provides a way to visualize and quantify changes in synaptic density, offering insights into the underlying pathology of the condition.25678

What is the purpose of this trial?

The purpose of this study is to utilize the radioactive positron emission tomography (PET) tracer \[11C\]UCB-J to test the neural synaptic pruning hypothesis of schizophrenia. This imaging method allows for the quantification of synaptic density in the living human brain and has the unprecedented ability to directly examine the synaptic pathology underlying neuropsychiatric disease. The neural synaptic pruning hypothesis posits that a key pathogenic process of schizophrenia is the over-exuberant elimination of neural synapses during development. The confirmation of reduced synaptic density in schizophrenia as evidenced by \[11C\]UCB-J has the potential to lead to a number of ground-breaking clinical innovations, such as laboratory-based diagnostics and prognostics, and novel, disease-modifying treatments.

Research Team

JH

Jong H Yoon, MD

Principal Investigator

Stanford University

Eligibility Criteria

This trial is for adults aged 18-65 with a clinical diagnosis of schizophrenia, schizophreniform, or schizoaffective disorder. Participants must be on stable medication for at least two weeks and able to undergo a PET-MR scan without sedation.

Inclusion Criteria

I have been diagnosed with schizophrenia or a related disorder.
I can undergo a PET-MR scan without needing sedation.
My medication has not changed in the last two weeks.

Timeline

Screening

Participants are screened for eligibility to participate in the trial

2-4 weeks

Imaging

Participants undergo positron emission tomography-magnetic resonance (PET-MR) imaging using the [11C]UCB-J radiotracer

120 minutes
1 visit (in-person)

Follow-up

Participants are monitored for safety and effectiveness after imaging

4 weeks

Treatment Details

Interventions

  • [11C]UCB-J radiotracer
Trial Overview The study uses [11C]UCB-J radiotracer in a PET-MR imaging technique to measure synaptic density in the brain and test the neural synaptic pruning hypothesis related to schizophrenia.
Participant Groups
2Treatment groups
Experimental Treatment
Group I: Schizophrenia (SZ) ParticipantsExperimental Treatment2 Interventions
Participants will undergo positron emission tomography-magnetic resonance (PET-MR) imaging using the \[11C\]UCB-J radiotracer
Group II: Healthy Control (HC) ParticipantsExperimental Treatment2 Interventions
Participants will undergo positron emission tomography-magnetic resonance (PET-MR) imaging using the \[11C\]UCB-J radiotracer

Find a Clinic Near You

Who Is Running the Clinical Trial?

Davidzon, Guido, M.D.

Lead Sponsor

Trials
3
Recruited
60+

Weston Havens Foundation

Collaborator

Trials
1
Recruited
60+

Findings from Research

A comprehensive review of 18 meta-analyses involving over 50,000 subjects indicates that schizophrenia is linked to lower grey matter volumes, cortical thickness, and abnormal brain structure, suggesting significant synaptic alterations.
Key brain regions affected include the frontal, anterior cingulate, and temporal cortices, as well as the hippocampi, with evidence pointing towards lower synaptic density in these areas compared to healthy controls.
Neuroimaging in schizophrenia: an overview of findings and their implications for synaptic changes.Howes, OD., Cummings, C., Chapman, GE., et al.[2023]
Patients with schizophrenia showed significantly lower synaptic vesicle density, as measured by the PET ligand [11C]UCB-J, across multiple brain regions compared to healthy controls, indicating a potential biomarker for the disease.
The study found that lower synaptic vesicle density in the frontal cortex was associated with more severe psychotic symptoms and poorer cognitive performance, suggesting a link between synaptic health and the severity of schizophrenia symptoms.
In vivo evidence of lower synaptic vesicle density in schizophrenia.Radhakrishnan, R., Skosnik, PD., Ranganathan, M., et al.[2023]
In a study involving 18 patients with schizophrenia and 18 controls, researchers found significantly lower levels of synaptic vesicle glycoprotein 2A (SV2A) in the frontal and anterior cingulate cortices of patients, suggesting a link between synaptic dysfunction and schizophrenia symptoms.
The study also showed that antipsychotic medications did not significantly affect SV2A levels in rats, indicating that the observed lower levels in schizophrenia are not due to medication effects.
Synaptic density marker SV2A is reduced in schizophrenia patients and unaffected by antipsychotics in rats.Onwordi, EC., Halff, EF., Whitehurst, T., et al.[2023]

References

Neuroimaging in schizophrenia: an overview of findings and their implications for synaptic changes. [2023]
In vivo evidence of lower synaptic vesicle density in schizophrenia. [2023]
Synaptic density marker SV2A is reduced in schizophrenia patients and unaffected by antipsychotics in rats. [2023]
Reductions in synaptic marker SV2A in early-course Schizophrenia. [2023]
Synaptic Terminal Density Early in the Course of Schizophrenia: An In Vivo UCB-J Positron Emission Tomographic Imaging Study of Synaptic Vesicle Glycoprotein 2A. [2023]
Validation and noninvasive kinetic modeling of [11C]UCB-J PET imaging in mice. [2021]
Synthesis and in vivo evaluation of [18F]UCB-J for PET imaging of synaptic vesicle glycoprotein 2A (SV2A). [2020]
Human adult and adolescent biodistribution and dosimetry of the synaptic vesicle glycoprotein 2A radioligand 11C-UCB-J. [2023]
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