Researchers report that restoring RAI1 gene expression levels during an early age-window partially reversed gene expression and social interaction deficits in a mouse model of Smith-Magenis syndrome (SMS), a neurodevelopmental disorder associated with insufficient RAI1 expression; optogenetic stimulation of prefrontal cortex neurons, which exhibited reduced dendritic spine density in RAI1-deficient mice, also partially reversed social interaction deficits, suggesting potential therapeutic strategies for SMS.
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Article #18-06796: "Early adolescent Rai1 reactivation reverses transcriptional and social interaction deficits in a mouse model of Smith-Magenis syndrome," by Wei-Hsiang Huang et al .
MEDIA CONTACT: Liqun Luo, Stanford University, CA; tel: 650-723-6645; e-mail: < lluo@stanford.edu >; Wei-Hsiang Huang, Stanford University, CA; email: weihsiah@stanford.edu
Proceedings of the National Academy of Sciences