https://www.selleckchem.com/Bcl-2.html
021) and CNVs (9 of 397 vs 24 of 562, p=0.065) compared with individuals who manifested both autism and ID (IQ less then 7. Pathogenic variants disrupting autism-associated genes conferred a 4.85-fold increased risk (p=0.011) for comorbid ID, while de novo variants observed in individuals with high-functioning autism disrupted genes with little functional relevance towards neurodevelopment. CONCLUSIONS Pathogenic de novo variants disrupting autism-associated genes contribute towards autism and ID comorbidity, while other genetic factors are like
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