Thalamic microRNA controls the late onset of schizophrenia (SJ-15-0035)

St. Jude Reference #SJ-15-0035


Researchers at St. Jude continued their work on the molecular mechanism that disrupts the flow of information along a neural circuit connecting two brain regions that process auditory information (SJ-15-0009), and also discovered clues about why psychotic symptoms of schizophrenia are often delayed until late adolescence or early adulthood in a mouse model that represents a genetic cause of schizophrenia. Researchers had previously identified the specific circuit in the brain that is targeted by antipsychotic drugs.

Existing antipsychotics also cause devastating side effects. The researchers, led by Stanislav Zakharenko, M.D., Ph.D. also discovered that miRNA is a key player in disruption of that circuit and showed that depletion of the miRNA was necessary and sufficient to inhibit normal functioning of the circuit in the mouse models, and they believe a miRNA named miR-338-3p could be targeted for development of a new class of antipsychotic drugs with fewer side effects to more effectively treat the hallucinations of schizophrenia caused by the disruption of information along neural pathways.


Schizophrenia, antipsychotic, miRNA, side effect, hallucinations, neurological disease

Granted patents or published applications

Issued US Patent 10,441,601; and pending US Patent 

Related scientific references

Thalamic miR-338-3p mediates auditory thalamocortical disruption and its late onset in 22q11.2 microdeletion models. Nature Medicine. Published online ahead of print: November 28, 2016. DOI: 10.1038/nm.4240

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