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Internalizing symptoms and social communication difficulties were most strongly associated with the cognitive-adaptive functioning gap, and SHAP analysis identified internalizing problems, social communication challenges, and OCD symptoms as the strongest predictors.
The first comprehensive human mechanistic model of PPP1R9A haploinsufficiency using an isogenic CRISPR/Cas9-engineered iPSC system differentiated into cortical neurons is established, providing a human-specific mechanistic framework linking reduced Neurabin I dosage to neurodevelopmental and psychiatric disease risk.
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