{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Walker A"],"funding":["Brain and Behavior Research Foundation Distinguished Investigator Grant, Swedish Research Council","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH)","Lundbeckfonden (Lundbeck Foundation)","NIMH NIH HHS","Lundbeckfonden","U.S. Department of Health &amp; Human Services | NIH | National Institute of Mental Health","Australian National Health and Medical Research Council"],"pagination":["2009-2016"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12014356"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["30(5)"],"pubmed_abstract":["This study represents the first large-scale investigation of rare (<1% population frequency) copy number variants (CNVs) in anorexia nervosa (AN). Large, rare CNVs are reported to be causally associated with anthropometric traits, neurodevelopmental disorders, and schizophrenia, yet their role in the genetic basis of AN is unclear. Using genome-wide association study (GWAS) array data from the Anorexia Nervosa Genetics Initiative (ANGI), which included 7414 AN case and 5044 controls, we investigated the association of 67 well-established syndromic CNVs and 178 pleiotropic disease-risk dosage-sensitive CNVs with AN. To identify novel CNV regions (CNVRs) that increase the risk of AN, we conducted genome-wide association studies with a focus on rare CNV-breakpoints (CNV-GWAS). We found no net"],"journal":["Molecular psychiatry"],"pubmed_title":["Genome-wide copy number variation association study in anorexia nervosa."],"pmcid":["PMC12014356"],"funding_grant_id":["R01 MH124871","R01 MH120170","R56 MH129437","R01MH136148; R56MH129437; R01MH120170; R01MH124871; R01MH118278; R01MH124871","R276-2018-4581","R01 MH118278","R01 MH121545","R01 MH136149"],"pubmed_authors":["McRae A","Baker JH","Woodside DB","Brandt H","Strober M","Thornton LM","Fundin BT","Martin NG","Wray NR","Lin T","Munn-Chernoff MA","Gordon S","Leppa VM","Sidorenko J","Halmi KA","Jordan J","Szatkiewicz JP","Wen J","Yilmaz Z","Walker A","Pedersen NL","Kirov G","Crawford S","Landen M","Sullivan PF","Berrettini WH","Parker R","Mitchell J","Borg S","Bulik CM","Watson HJ","Davies HL","Song J","Kennedy MA","Savva A","Chawner SJRA","Birgegard A","Karlsson R","Kaplan AS","Kaye WH"],"additional_accession":[]},"is_claimable":false,"name":"Genome-wide copy number variation association study in anorexia nervosa.","description":"This study represents the first large-scale investigation of rare (<1% population frequency) copy number variants (CNVs) in anorexia nervosa (AN). Large, rare CNVs are reported to be causally associated with anthropometric traits, neurodevelopmental disorders, and schizophrenia, yet their role in the genetic basis of AN is unclear. Using genome-wide association study (GWAS) array data from the Anorexia Nervosa Genetics Initiative (ANGI), which included 7414 AN case and 5044 controls, we investigated the association of 67 well-established syndromic CNVs and 178 pleiotropic disease-risk dosage-sensitive CNVs with AN. To identify novel CNV regions (CNVRs) that increase the risk of AN, we conducted genome-wide association studies with a focus on rare CNV-breakpoints (CNV-GWAS). We found no net","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-02T00:06:15.289Z","creation":"2025-07-08T03:12:48.303Z"},"accession":"S-EPMC12014356","cross_references":{"pubmed":["39533101"],"doi":["10.1038/s41380-024-02811-2"]}}