Together, these findings anchor ASD genetic vulnerability to specific neurodevelopmental lineages, epochs, and molecular substrates, and delineate the features that distinguish ASD from comorbidities with broader developmental impacts.
Rachel L. Smith, Yun-Dan Liao, L. Klei et al.· bioRxiv· 0 citations
It is found that damaging de novo single-nucleotide variants and frameshift indels explain 3.4% (95% CI: 2.1% - 4.7%) of autism variance on the observed scale.
A. Nadig, J. Fu, F. Satterstrom et al.· medRxiv· 0 citations
This study finds that rare variants across hundreds of genes contribute to autism with variable phenotypic outcomes, and clusters them based on association evidence from large-scale studies of developmental disorders, schizophrenia, bipolar disorder, and epilepsy.
F. Satterstrom, C. Auwerx, J.-M. Fu et al.· medRxiv· 1 citation
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