ArticleMolecular autism2011
The ongoing dissection of the genetic architecture of autistic spectrum disorder.
Article in Molecular autism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Common functional variants of the glutamatergic system in Autism spectrum disorder with high and low intellectual abilities.Journal of neural transmission (Vienna, Austria : 1996) · 2018Article
- Polymorphism in the Promoter Region ofPsychiatry investigation · 2017Article
- Subthreshold traits of the broad autistic spectrum are distributed across different subgroups in parents, but not siblings, of probands with autism.European child & adolescent psychiatry · 2014Article
- Transcriptomic analysis of genetically defined autism candidate genes reveals common mechanisms of action.Molecular autism · 2013Article
- Epigenetics and autism.Autism research and treatment · 2013Review
- A review of the evidence for the canonical Wnt pathway in autism spectrum disorders.Molecular autism · 2012Article
- Neural mechanisms of social risk for psychiatric disorders.Nature neuroscience · 2012Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of robust, non-hypothesis based case/control studies has led to a large push forward towards identifying common genetic variants that contribute to complex traits. However, despite many attempts, the search for common disease-predisposing variants in childhood developmental disorders has largely failed. Recently, a role for rare causal variants and de novo mutations is emerging in the genetic architecture of some of these disorders, particularly those that incur a large degree of selection against the phenotype. In this paper, we examine these data and use classic genetic epidemiological approaches to gain insights into the genetic architecture of ASD. Future studies using next generation sequencing should elucidate the precise role de novo mutations play in disorders traditionally thought to have resulted from polygenic or common disease, common variants inheritance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.