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Laboratory validation yielded a sensitivity of 82% (85% for high\u2010quality).<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>We found a burden of singletons (odds ratio [OR]\u00a0=\u00a01.07, <jats:italic>p<\/jats:italic>\u00a0=\u00a00.0017) and homozygous deletions (OR\u00a0=\u00a01.14, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.0001) in cases. On AD genes, we observed the ultra\u2010rare SVs associated with the disease, including protein\u2010altering SVs in <jats:italic>ABCA7<\/jats:italic>, <jats:italic>APP<\/jats:italic>, <jats:italic>PLCG2<\/jats:italic>, and <jats:italic>SORL1<\/jats:italic>. Twenty\u2010one SVs are in linkage disequilibrium (LD) with known AD\u2010risk variants, exemplified by a 5k deletion in LD (<jats:italic>R<\/jats:italic><jats:sup>2<\/jats:sup>\u00a0=\u00a00.99) with rs143080277 in <jats:italic>NCK2<\/jats:italic>. We identified a rare deletion near <jats:italic>RNA5SP293<\/jats:italic> associated with AD (OR\u00a0=\u00a01.99, <jats:italic>p<\/jats:italic>\u00a0=\u00a01.3\u00a0\u00d7\u00a010<jats:sup>\u22125<\/jats:sup>), which was replicated using an independent dataset.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>This study highlights the pivotal role of SVs in AD genetics.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Observed a significant burden of singletons and homozygous deletions in Alzheimer's disease (AD) patients.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Identified rare protein\u2010altering structural variations (SVs) in ABCA7, APP, PLCG2, and SORL1.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Established linkages between SVs and AD risk\u2010associated single nucleotide variants (SNVs).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Discovered a novel deletion near <jats:italic>RNA5SP293<\/jats:italic> linked to AD, replicated independently.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Uncovered over\u2010representation of SVs in neuronal function pathways.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.70277","type":"journal-article","created":{"date-parts":[[2025,6,17]],"date-time":"2025-06-17T23:55:45Z","timestamp":1750204545000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Structural variation detection and association analysis of whole\u2010genome\u2010sequence data from 16,543 Alzheimer's disease sequencing project subjects"],"prefix":"10.1002","volume":"21","author":[{"given":"Hui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine Perelman School of Medicine University 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