ArticleMolecular psychiatry2009
A high-density SNP genome-wide linkage scan in a large autism extended pedigree.
Article in Molecular psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
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- AMPD1 functional variants associated with autism in Han Chinese population.European archives of psychiatry and clinical neuroscience · 2015Article
- Protein tyrosine phosphatase PTPRT as a regulator of synaptic formation and neuronal development.BMB reports · 2015Review
- Inactivation of the catalytic phosphatase domain of PTPRT/RPTPρ increases social interaction in mice.Autism research : official journal of the International Society for Autism Research · 2015Article
- Using extended pedigrees to identify novel autism spectrum disorder (ASD) candidate genes.Human genetics · 2015Article
- Epigenetic remodelling and dysregulation of DLGAP4 is linked with early-onset cerebellar ataxia.Human molecular genetics · 2014Article
- Common genetic variants on 1p13.2 associate with risk of autism.Molecular psychiatry · 2014Article
- Quantitative linkage for autism spectrum disorders symptoms in attention-deficit/hyperactivity disorder: significant locus on chromosome 7q11.Journal of autism and developmental disorders · 2014Article
- Adult expression of a 3q13.31 microdeletion.Molecular cytogenetics · 2014Article
- Identification of rare DNA sequence variants in high-risk autism families and their prevalence in a large case/control population.Molecular autism · 2014Article
- Developmental and adult GAP-43 deficiency in mice dynamically alters hippocampal neurogenesis and mossy fiber volume.Developmental neuroscience · 2014Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
We performed a high-density, single nucleotide polymorphism (SNP), genome-wide scan on a six-generation pedigree from Utah with seven affected males, diagnosed with autism spectrum disorder. Using a two-stage linkage design, we first performed a nonparametric analysis on the entire genome using a 10K SNP chip to identify potential regions of interest. To confirm potentially interesting regions, we eliminated SNPs in high linkage disequilibrium (LD) using a principal components analysis (PCA) method and repeated the linkage results. Three regions met genome-wide significance criteria after controlling for LD: 3q13.2-q13.31 (nonparametric linkage (NPL), 5.58), 3q26.31-q27.3 (NPL, 4.85) and 20q11.21-q13.12 (NPL, 5.56). Two regions met suggestive criteria for significance 7p14.1-p11.22 (NPL, 3.18) and 9p24.3 (NPL, 3.44). All five chromosomal regions are consistent with other published findings. Haplotype sharing results showed that five of the affected subjects shared more than a single chromosomal region of interest with other affected subjects. Although no common autism susceptibility genes were found for all seven autism cases, these results suggest that multiple genetic loci within these regions may contribute to the autism phenotype in this family, and further follow-up of these chromosomal regions is warranted.
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