Tissue- and cell-type-specific molecular and functional signatures of 16p11.2 reciprocal genomic disorder across mouse brain and human neuronal models.

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This study used mouse brain tissue and human brain cell models to explore how 16p11.2 deletions and duplications change gene activity and brain cell development, discovering that these genetic changes disrupt the balance between excitatory and inhibitory brain cells—a finding that may help explain learning, behavioral, and developmental differences seen in children and adults with 16p11.2 conditions.