A Genome‐wide Association Study of Autism Reveals a Common Novel Risk Locus at 5p14.1
Open accessAbstract
Summary: Although autism is one of the most heritable neuropsychiatric disorders, its underlying genetic architecture has largely eluded description. To comprehensively examine the hypothesis that common variation is important in autism, we performed a genome‐wide association study (GWAS) using a discovery dataset of 438 autistic Caucasian families and the Illumina Human 1M beadchip. 96 single nucleotide polymorphisms (SNPs) demonstrated strong association with autism risk (p‐value < 0.0001). The validation of the top 96 SNPs was performed using an independent dataset of 487 Caucasian autism families genotyped on the 550K Illumina BeadChip. A novel region on chromosome 5p14.1 showed significance in both the discovery and validation datasets. Joint analysis of all SNPs in this region identified 8 SNPs having improved p‐values (3.24E‐04 to 3.40E‐06) than in either dataset alone. Our findings demonstrate that in addition to multiple rare variations, part of the complex genetic architecture of autism involves common variation.
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The largest GWAS to date (n=7387 cases scanned) did not conclusively identify single variants at genome-wide significance.
“the largest GWAS to date (n=7387 cases scanned) -while providing compelling evidence for the bulk contribution of common variants -did not conclusively identify single variants at genome-wide significance 5-7 .”
From Identification of common genetic risk variants for autism spectrum disorder (2019) · cites this paper as [6]
The Results (page not provided) report that no association in this study met genome-wide significance, supporting that part of the claim. But the paper reports 438 discovery families and 457 validation families, not 7,387 cases, and does not identify its study as the largest GWAS to date. The Discussion (page not provided) also notes that combining its data with two additional datasets yielded SNP associations that survived Bonferroni correction. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe study reports the first common risk variants robustly associated with ASD by more than doubling the discovery sample size compared to previous GWAS.
“Here we report the first common risk variants robustly associated with ASD by more than doubling the discovery sample size compared to previous GWAS 5-8 .”
From Identification of common genetic risk variants for autism spectrum disorder (2019) · cites this paper as [6]
ASD genomewide association studies have not identified reproducible SNP associations.
“and have failed to identify reproducible SNP associations (16)(17)(18)(19)(20).”
From Genetics and genomics of autism spectrum disorder: embracing complexity (2015) · cites this paper as [18]
Our results from >2700 trios, together with the results from other published GWAS, bear out the prediction that few if any common variants have an impact on risk exceeding 1.2.
“Our results from >2700 trios, together with the results from other published GWAS (22,23,34), bear out this prediction.”
From Individual common variants exert weak effects on the risk for autism spectrum disorders (2012) · cites this paper as [34]
Early ASD GWAS had low statistical power to robustly identify genome-wide significant loci at effect sizes OR < 1.15.
“Early GWAS [12, 14–17] were performed using a variety of genotyping arrays, and the independent samples sizes were of low statistical power to robustly identify genome-wide significant (GWS) loci at the lower effect sizes (OR <1.15) [18].”
Voineagu et al. identified a gene expression module that had attenuated expression in post-mortem brain samples of individuals with ASD and which also had enrichment for GWAS signals.
“Additional support for our recommendation for more GWAS is provided by Voineagu et al. who identified a gene expression module that had attenuated expression in post-mortem brain samples of individuals with ASD and which also had enrichment for GWAS signals. 90”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [90]
An empirically-derived gene expression module that is under-expressed in ASD was found to be enriched for known ASD susceptibility genes and genetic association signals.
“and an empirically-derived gene expression module that is under-expressed in ASD was found to be enriched for known ASD susceptibility genes and genetic association signals. 90”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [90]
For ASD, typical patterns of cortical gene expression in frontal and temporal cortex have been found to be attenuated in ASD cases compared to controls.
“For ASD, typical patterns of cortical gene expression in frontal and temporal cortex have been found to be attenuated in ASD cases compared to controls”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [90]
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- Authors
- Ma, D., Salyakina, D., Jaworski, J. M., Konidari, I., Whitehead, P. L., Andersen, A. N., Hoffman, J. D., Slifer, S. H., Hedges, D. J., Cukier, H. N., Griswold, A. J., McCauley, J. L., Beecham, G. W., Wright, H. H., Abramson, R. K., Martin, E. R., Hussman, J. P., Gilbert, J. R., Cuccaro, M. L., Haines, J. L., & Pericak‐Vance, M. A.
- Affiliations
- University of Miami (US)
- University of South Carolina (US)
- John P. Hussman Foundation (US)
- Vanderbilt University Medical Center (US)
- Corresponding author
- Haines, Jonathan L.
- Pericak‐Vance, Margaret A.
- ORCID
- Venue
- Annals of Human Genetics
- Publisher
- Wiley
- Published
- 2009-04-28
- Volume
- 73
- Issue
- 3
- Pages
- 263-273
- ISSN
- 0003-4800 (ISSN-L)
- 1469-1809
- PMC
- PMC2918410
- OpenAlex
- W1993360322
- Cited by
- 221
- References
- 33
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 8 · 2020: 11 · 2019: 11 · 2018: 7 · 2017: 21 · 2016: 11 · 2015: 12 · 2014: 22 · 2013: 17 · 2012: 25
- FWCI
- 13.71
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Human Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Vanderbilt University
- Hussman Foundation
- National Institutes of Health
- National Institute of Mental Health (R01MH080647, MH080647)
- National Institute of General Medical Sciences (T32GM080178)
- National Institute of Neurological Disorders and Stroke (P01NS026630, NS36768, R01NS036768, NS 26630)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- autism spectrum disorder, genetic susceptibility loci, common genetic variants, single nucleotide polymorphisms, genetic architecture, neuropsychiatric disorders, family-based association
- MeSH terms
- Adolescent, Autistic Disorder, Child, Child, Preschool, Chromosomes, Human, Pair 5, Female, Humans, Male, Pedigree, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, White People, Genome-Wide Association Study, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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