ArticleMolecular psychiatry2011
A genome-wide association study on common SNPs and rare CNVs in anorexia nervosa.
Article in Molecular psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 6 of them syntheses that pooled it.
What it found
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Who cites it
109 citing papers in PubMed, 6 syntheses or guidelines pooled it, 216 citations in OpenAlex.
- Integrative GWAS identifies novel loci and genetic links between psychiatric and metabolic factors in anorexia nervosa.Molecular psychiatry · 2026Pooled it
- Brain-based gene expression of putative risk genes for anorexia nervosa.Molecular psychiatry · 2023Pooled it
- Mental health dished up-the use of iPSC models in neuropsychiatric research.Journal of neural transmission (Vienna, Austria : 1996) · 2020Pooled it
- Examination of the shared genetic basis of anorexia nervosa and obsessive-compulsive disorder.Molecular psychiatry · 2020Pooled it
- Significant Locus and Metabolic Genetic Correlations Revealed in Genome-Wide Association Study of Anorexia Nervosa.The American journal of psychiatry · 2017Pooled it
- Genetic contributions to variation in general cognitive function: a meta-analysis of genome-wide association studies in the CHARGE consortium (N=53949).Molecular psychiatry · 2015Pooled it
- Shared and distinct genetic architectures of eating disorders and obesity: From monogenic causes to polygenic risk.Reviews in endocrine & metabolic disorders · 2026Review
- CNTN6 Modulates Slit-Robo Signaling in Cortical GABAergic Interneuron Migration.Neuroscience bulletin · 2026Article
- Convergent molecular signatures across eating disorders and obsessive-compulsive disorder in the human brain.Cell reports · 2026Article
- Role of CNTN6 in neurodevelopment and neuropathology.Frontiers in neuroscience · 2026Review
- Genomic meta-analyses of binge-eating behavior and anorexia nervosa yield insights into the unique and shared biology of eating disorder phenotypes.Nature. Mental health · 2026Article
- Utilising genomic association data for causal inference in anorexia nervosa.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Polygenicity at the pathway level for anorexia nervosa.medRxiv : the preprint server for health sciences · 2025Article
- Shared genetic architecture between eating disorders, mental health conditions, and cardiometabolic diseases: a comprehensive population-wide study across two countries.Nature communications · 2025Article
- Genetics of Anorexia Nervosa: Translation to Future Personalized Therapies.The Psychiatric clinics of North America · 2025Review
- Genome-wide copy number variation association study in anorexia nervosa.Molecular psychiatry · 2025Article
- Endogenous opioid receptors and the feast or famine of maladaptive feeding.Nature communications · 2025Review
- Application of Genetic Testing for Anorexia Nervosa: An Ethical Analysis.Brain and behavior · 2025Article
- Eating behaviour and eating disorders in individuals with rare neurodevelopmental variants: current knowledge and future research directions.Frontiers in psychiatry · 2025Article
- Convergent molecular signatures across eating disorders and obsessive-compulsive disorder in the human brain.medRxiv : the preprint server for health sciences · 2024Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Anorexia nervosa (AN) is a mental illness with high mortality that most commonly afflicts adolescent female individuals. Clinical symptoms include chronic food refusal, weight loss and body image distortions. We carried out a genome-wide association study on 1033 AN cases and 3733 pediatric control subjects, all of whom were of European ancestry and were genotyped on the Illumina HumanHap610 platform (Illumina, San Diego, CA, USA). We confirmed that common single-nucleotide polymorphisms (SNPs) within OPRD1 (rs533123, P=0.0015) confer risk for AN, and obtained suggestive evidence that common SNPs near HTR1D (rs7532266, P=0.04) confer risk for restricting-type AN specifically. However, no SNPs reached genome-wide significance in our data, whereas top association signals were detected near ZNF804B, CSRP2BP, NTNG1, AKAP6 and CDH9. In parallel, we performed genome-wide analysis on copy number variations (CNVs) using the signal intensity data from the SNP arrays. We did not find evidence that AN cases have more CNVs than control subjects, nor do they have over-representation of rare or large CNVs. However, we identified several regions with rare CNVs that were only observed in AN cases, including a recurrent 13q12 deletion (1.5 Mb) disrupting SCAS in two cases, and CNVs disrupting the CNTN6/CNTN4 region in several AN cases. In conclusion, our study suggests that both common SNPs and rare CNVs may confer genetic risk to AN. These results point to intriguing genes that await further validation in independent cohorts for confirmatory roles in AN.
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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.