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Consequently, causal variants for most PD risk are not known. Here we focused on structural variants (SVs), which represent a major source of genetic variation in the human genome. We aimed to discover SVs associated with PD risk by performing the first large\u2010scale characterization of SVs in PD.<\/jats:p><\/jats:sec>Methods<\/jats:title>We leveraged a recently developed computational pipeline to detect and genotype SVs from 7,772 Illumina short\u2010read whole genome sequencing samples. Using this set of SV variants, we performed a genome\u2010wide association study using 2,585 cases and 2,779 controls and identified SVs associated with PD risk. Furthermore, to validate the presence of these variants, we generated a subset of matched whole\u2010genome long\u2010read sequencing data.<\/jats:p><\/jats:sec>Results<\/jats:title>We genotyped and tested 3,154 common SVs, representing over 412 million nucleotides of previously uncatalogued genetic variation. Using long\u2010read sequencing data, we validated the presence of three novel deletion SVs that are associated with risk of PD from our initial association analysis, including a 2\u00a0kb intronic deletion within the gene LRRN4<\/jats:italic>.<\/jats:p><\/jats:sec>Interpretation<\/jats:title>We identified three SVs associated with genetic risk of PD. This study represents the most comprehensive assessment of the contribution of SVs to the genetic risk of PD to date. 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