St. Jude Reference #SJ-19-0048
Description
Cognitive symptoms involving social abnormalities are prevalent in several neuropsychiatric diseases such as autism and schizophrenia. Researchers at St. Jude determined the social deficit is not due to a decrease in sociability; but by genetics tied to social recognition and memory. Manipulating the cascade of genes that we discovered could be a therapeutic avenue for treating social memory deficits in these diseases.
Researchers at St. Jude have discovered a novel gene and molecular mechanism that underlies a complex behavior, called social (or recognition) memory. This memory is shown to be encoded in the hippocampus, but the molecular mechanisms were unknown. What was known is that mouse models of 22q11 deletion syndrome were deficient in this memory. Because 22q11DS is caused by deletion of more than 20 genes, the culprit gene was a mystery. The researchers found a specific gene, a gene of previously unknown function- 2510002D24Rik- was shown to be involved with the negative symptom (poor or non-existant social functioning). The 2510002D24Rik-encoded protein is localized to mitochondria and interacts with Atp23. Replenishing Atp23 in 2510002D24Rik negative mice rescues the phenotype.
Keywords
Social abnormality, Neuropsychiatric, Autism, Schizophrenia, Social (or recognition) memory, hippocampus, 22q11 deletion syndrome
Granted patents or published applications
Pending US patent published as US 2022/0288235 A1
Related scientific references
Licensing opportunities
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