Michelle Dawson posts

Post published on Bluesky on 10 Jul 2025 12:01

Bluesky DOI work crossref Extract quoted in the post Question asked by Dawson in the post External link integrated into the post Autism terms

Authors create 4 classes of autism?--"Social/behavioral" (37%), "Mixed ASD with DD" (19%), "Moderate challenges" (34%), "Broadly affected" (10%)? www.nature.com/articles/s41... based on SCQ, CBCL, & RBS-R scores & developmental milestones, in N=5392 autistics aged 4-18 years, free

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DOI work Fetched Post crossref

Aviya Litman, Natalie Sauerwald, LeeAnne Green Snyder, Jennifer Foss-Feig, Christopher Y. Park, Yun Hao, Ilan Dinstein, Chandra L. Theesfeld, et al. (2025). Decomposition of phenotypic heterogeneity in autism reveals underlying genetic programs. Nature Genetics, 57(7), 1611-1619. Springer Science and Business Media LLC.

Publication date
9 Jul 2025
Identifier
10.1038/s41588-025-02224-z
Authors
Aviya Litman, Natalie Sauerwald, LeeAnne Green Snyder, Jennifer Foss-Feig, Christopher Y. Park, Yun Hao, Ilan Dinstein, Chandra L. Theesfeld, Olga G. Troyanskaya
Source
Nature Genetics
Details
57(7), 1611-1619
Reference type
article
Publisher
Springer Science and Business Media LLC
Metadata source
crossref

Abstract

Abstract Unraveling the phenotypic and genetic complexity of autism is extremely challenging yet critical for understanding the biology, inheritance, trajectory and clinical manifestations of the many forms of the condition. Using a generative mixture modeling approach, we leverage broad phenotypic data from a large cohort with matched genetics to identify robust, clinically relevant classes of autism and their patterns of core, associated and co-occurring traits, which we further validate and replicate in an independent cohort. We demonstrate that phenotypic and clinical outcomes correspond to genetic and molecular programs of common, de novo and inherited variation and further characterize distinct pathways disrupted by the sets of mutations in each class. Remarkably, we discover that class-specific differences in the developmental timing of affected genes align with clinical outcome differences. These analyses demonstrate the phenotypic complexity of children with autism, identify genetic programs underlying their heterogeneity, and suggest specific biological dysregulation patterns and mechanistic hypotheses.

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