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Members of 67 <jats:styled-content style=\"fixed-case\">CH<\/jats:styled-content> and additional 47 Caucasian families underwent <jats:styled-content style=\"fixed-case\">WGS<\/jats:styled-content> as a part of the Alzheimer's Disease Sequencing Project (<jats:styled-content style=\"fixed-case\">ADSP<\/jats:styled-content>). All members of 67 <jats:styled-content style=\"fixed-case\">CH<\/jats:styled-content> families, an additional 48 <jats:styled-content style=\"fixed-case\">CH<\/jats:styled-content> families and an independent <jats:styled-content style=\"fixed-case\">CH<\/jats:styled-content> case\u2010control cohort were subsequently genotyped for validation. Patients met criteria for <jats:styled-content style=\"fixed-case\">LOAD<\/jats:styled-content>, and controls were determined to be dementia free. We investigated rare variants segregating within families and gene\u2010based associations with disease within <jats:styled-content style=\"fixed-case\">LOAD GWAS<\/jats:styled-content> loci.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A variant in <jats:italic><jats:styled-content style=\"fixed-case\">AKAP<\/jats:styled-content>9,<\/jats:italic> p.R434W, segregated significantly with <jats:styled-content style=\"fixed-case\">LOAD<\/jats:styled-content> in two large families (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content> = 5.77, 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>: 1.07\u201330.9, <jats:italic>P<\/jats:italic> = 0.041). In addition, missense mutations in <jats:italic><jats:styled-content style=\"fixed-case\">MYRF<\/jats:styled-content><\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">ASRGL<\/jats:styled-content>1<\/jats:italic> under previously reported linkage peaks at 7q14.3 and 11q12.3 segregated completely in one family and in follow\u2010up genotyping both were nominally significant (<jats:italic>P<\/jats:italic> &lt; 0.05). We also identified rare variants in a number of genes associated with <jats:styled-content style=\"fixed-case\">LOAD<\/jats:styled-content> in prior genome wide association studies, including <jats:italic><jats:styled-content style=\"fixed-case\">CR<\/jats:styled-content>1<\/jats:italic> (<jats:italic>P<\/jats:italic> = 0.049), <jats:italic><jats:styled-content style=\"fixed-case\">BIN<\/jats:styled-content>1<\/jats:italic> (<jats:italic>P<\/jats:italic> = 0.0098) and <jats:italic><jats:styled-content style=\"fixed-case\">SLC<\/jats:styled-content>24A4<\/jats:italic> (<jats:italic>P<\/jats:italic> = 0.040).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Relevance<\/jats:title><jats:p>Rare variants in multiple genes influence the risk of <jats:styled-content style=\"fixed-case\">LOAD<\/jats:styled-content> disease in multiplex families. These results suggest that rare variants may underlie loci identified in genome wide association studies.<\/jats:p><\/jats:sec>","DOI":"10.1002\/acn3.537","type":"journal-article","created":{"date-parts":[[2018,3,15]],"date-time":"2018-03-15T07:32:54Z","timestamp":1521099174000},"page":"406-417","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Whole genome sequencing of Caribbean Hispanic families with late\u2010onset Alzheimer's disease"],"prefix":"10.1002","volume":"5","author":[{"given":"Badri N.","family":"Vardarajan","sequence":"first","affiliation":[{"name":"The Taub Institute for Research on Alzheimer's Disease and the Aging Brain New York"},{"name":"The Gertrude H. 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