ArticleFrontiers in genetics2014
A scoring strategy combining statistics and functional genomics supports a possible role for common polygenic variation in autism.
Article in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Early Life Experiences Moderate the Relationship Between Genetic Risk of Autism and Current and Lifetime Mental Health.Frontiers in psychiatry · 2021Article
- Developmental neurogenetics and multimodal neuroimaging of sex differences in autism.Brain imaging and behavior · 2017Review
- Bio-collections in autism research.Molecular autism · 2017Review
- TAF1 Variants Are Associated with Dysmorphic Features, Intellectual Disability, and Neurological Manifestations.American journal of human genetics · 2015Article
- Genetic testing and autism: Tutorial for communication sciences and disorders.Journal of communication disordersArticle
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Authors and funding
13 authors.
Funding
Abstract
Autism spectrum disorders (ASD) are highly heritable complex neurodevelopmental disorders with a 4:1 male: female ratio. Common genetic variation could explain 40-60% of the variance in liability to autism. Because of their small effect, genome-wide association studies (GWASs) have only identified a small number of individual single-nucleotide polymorphisms (SNPs). To increase the power of GWASs in complex disorders, methods like convergent functional genomics (CFG) have emerged to extract true association signals from noise and to identify and prioritize genes from SNPs using a scoring strategy combining statistics and functional genomics. We adapted and applied this approach to analyze data from a GWAS performed on families with multiple children affected with autism from Autism Speaks Autism Genetic Resource Exchange (AGRE). We identified a set of 133 candidate markers that were localized in or close to genes with functional relevance in ASD from a discovery population (545 multiplex families); a gender specific genetic score (GS) based on these common variants explained 1% (P = 0.01 in males) and 5% (P = 8.7 × 10(-7) in females) of genetic variance in an independent sample of multiplex families. Overall, our work demonstrates that prioritization of GWAS data based on functional genomics identified common variants associated with autism and provided additional support for a common polygenic background in autism.
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