Reversal of synaptic and behavioral deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4.

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Researchers studying mice with the 16p11.2 duplication found that restoring a brain protein called Npas4—which regulates calming (GABA) signals in the prefrontal cortex—reversed social and learning difficulties, suggesting this pathway could be a future treatment target for children with the duplication.