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Of interest, one patient was found to carry a homozygous <jats:italic>C9orf72<\/jats:italic> expansion, while another carried both a <jats:italic>C9orf72<\/jats:italic> expansion and a <jats:italic>GRN<\/jats:italic> pathogenic variant. We also identified likely pathogenic variants in the TAR DNA binding protein (<jats:italic>TARDBP<\/jats:italic>), presenilin 1 (<jats:italic>PSEN1<\/jats:italic>), and valosin containing protein (<jats:italic>VCP<\/jats:italic>) genes, and a subset of variants of unknown significance in other rare FTD genes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>Our study reports the genetic characterization of a large FTD series and supports an unbiased sequencing screen, irrespective of clinical presentation or family history.<\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.12011","type":"journal-article","created":{"date-parts":[[2020,1,16]],"date-time":"2020-01-16T10:19:58Z","timestamp":1579169998000},"page":"118-130","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":82,"title":["Genetic screening of a large series of North American sporadic and familial frontotemporal dementia 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