<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bustos BI</submitter><funding>National Institute of Neurological Disorders and Stroke</funding><funding>National Institute of Environmental Health Sciences</funding><funding>Intramural NIH HHS</funding><funding>NIA NIH HHS</funding><funding>Simpson Querrey Center for Neurogenetics</funding><funding>Department of Health and Human Services</funding><funding>Intramural Research Programs of the National Institute of Neurological Disorders and Stroke</funding><funding>National Institute of Environmental Health Sciences,</funding><funding>National Institutes of Health</funding><funding>Department of Defense</funding><funding>National Institute on Aging</funding><funding>Michael J Fox Foundation for Parkinson's Research</funding><funding>NIH HHS</funding><funding>Michael J Fox Foundation for Parkinson’s Research</funding><pagination>65-74</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10060720</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>146(1)</volume><pubmed_abstract>Parkinson's disease is a complex neurodegenerative disorder with a strong genetic component, for which most known disease-associated variants are single nucleotide polymorphisms (SNPs) and small insertions and deletions (indels). DNA repetitive elements account for >50% of the human genome; however, little is known of their contribution to Parkinson's disease aetiology. While select short tandem repeats (STRs) within candidate genes have been studied in Parkinson's disease, their genome-wide contribution remains unknown. Here we present the first genome-wide association study of STRs in Parkinson's disease. Through a meta-analysis of 16 imputed genome-wide association study cohorts from the International Parkinson's Disease Genomic Consortium (IPDGC), totalling 39 087 individuals (16 642 c</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Genome-wide contribution of common short-tandem repeats to Parkinson's disease genetic risk.</pubmed_title><pmcid>PMC10060720</pmcid><funding_grant_id>Z01-AG000949-02</funding_grant_id><funding_grant_id>Z01 AG000949</funding_grant_id><funding_grant_id>Z01 ES101986</funding_grant_id><funding_grant_id>1ZIA-NS003154</funding_grant_id><funding_grant_id>Z01-ES101986</funding_grant_id><funding_grant_id>W81XWH-09-2-0128</funding_grant_id><pubmed_authors>Gibbs JR</pubmed_authors><pubmed_authors>Bustos BI</pubmed_authors><pubmed_authors>Gan-Or Z</pubmed_authors><pubmed_authors>Singleton AB</pubmed_authors><pubmed_authors>Krainc D</pubmed_authors><pubmed_authors>Lubbe SJ</pubmed_authors><pubmed_authors>Billingsley K</pubmed_authors><pubmed_authors>Blauwendraat C</pubmed_authors><pubmed_authors>International Parkinson’s Disease Genomics Consortium (IPDGC)</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome-wide contribution of common short-tandem repeats to Parkinson's disease genetic risk.</name><description>Parkinson's disease is a complex neurodegenerative disorder with a strong genetic component, for which most known disease-associated variants are single nucleotide polymorphisms (SNPs) and small insertions and deletions (indels). DNA repetitive elements account for >50% of the human genome; however, little is known of their contribution to Parkinson's disease aetiology. While select short tandem repeats (STRs) within candidate genes have been studied in Parkinson's disease, their genome-wide contribution remains unknown. Here we present the first genome-wide association study of STRs in Parkinson's disease. Through a meta-analysis of 16 imputed genome-wide association study cohorts from the International Parkinson's Disease Genomic Consortium (IPDGC), totalling 39 087 individuals (16 642 c</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-05-15T03:20:26.989Z</modification><creation>2025-02-19T02:23:29.029Z</creation></dates><accession>S-EPMC10060720</accession><cross_references><pubmed>36347471</pubmed><doi>10.1093/brain/awac301</doi></cross_references></HashMap>