How disrupted brain connections may cause hearing voices in people with 22q11.2 or 3q29 microdeletions
Thalamocortical disruption as a convergence point for schizophrenia risks
Looks at whether weakened connections between the thalamus and auditory cortex can explain hearing voices in adolescents and young adults with 22q11.2 or 3q29 microdeletions.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | St. Jude Children's Research Hospital NIH-funded |
| Lab location | 1 site (Memphis, United States) |
| Project ID | NIH-11311932 on NIH RePORTER |
What this research studies
From a patient's perspective, this work uses mouse models that carry the same 22q11.2 or 3q29 microdeletions linked to high schizophrenia risk to study brain wiring linked to auditory hallucinations. Researchers will examine thalamocortical connections between the auditory thalamus and auditory cortex using techniques like two-photon imaging, electrophysiology, and acoustic stimulation at ages that match late adolescence/early adulthood. The team will compare when and how these synaptic disruptions arise and look for cellular signs that predict positive psychotic-like symptoms. The goal is to find measurable brain changes that could point toward new ways to prevent or treat hearing voices.
Who could benefit from this research
Good fit: People with a confirmed 22q11.2 deletion or 3q29 microdeletion—especially adolescents or young adults at risk for or beginning to experience psychotic symptoms—are the patients most likely to benefit from future clinical steps based on this research.
Not a fit: Patients expecting an immediate new treatment should not expect direct benefit, and individuals whose psychotic symptoms arise from unrelated causes or different brain mechanisms may not benefit from findings specific to these microdeletions.
Why it matters
Potential benefit: If successful, this work could reveal specific brain circuit changes to target for new treatments that prevent or reduce auditory hallucinations in people with these high-risk microdeletions and possibly broader schizophrenia.
How similar studies have performed: Previous mouse work, including prior studies by this group, has shown thalamocortical synaptic disruptions in 22q11DS models, but translating those findings into proven human treatments remains unproven.
Where this research is happening
Memphis, United States
- St. Jude Children's Research Hospital — Memphis, United States (Active)
Researchers
- Principal investigator: Zakharenko, Stanislav S — St. Jude Children's Research Hospital
- Study coordinator: Zakharenko, Stanislav S
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.