{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T15:57:36Z","timestamp":1788796656405,"version":"build-2803163510"},"reference-count":106,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,8,16]],"date-time":"2024-08-16T00:00:00Z","timestamp":1723766400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2024,8,16]],"date-time":"2024-08-16T00:00:00Z","timestamp":1723766400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["movementdisorders.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Progressive supranuclear palsy (PSP) is largely a sporadic disease with few reported familial cases. Genome\u2010wide association studies (GWAS) in sporadic PSP in Caucasian populations have identified\n                      <jats:italic>MAPT<\/jats:italic>\n                      as the most commonly associated genetic risk locus with the strongest effect size. At present there are limited data on genetic factors associated with PSP in Asian populations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Our goal was to investigate the genetic factors associated with PSP in Southeast Asian PSP patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Next\u2010generation sequencing (whole\u2010exome, whole\u2010genome and targeted sequencing) was performed in two Asian cohorts, comprising 177 PSP patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified 17 pathogenic or likely pathogenic variants in 16 PSP patients (9%), eight of which were novel. The most common relevant genetic variants identified were in\n                      <jats:italic>MAPT<\/jats:italic>\n                      ,\n                      <jats:italic>GBA1<\/jats:italic>\n                      ,\n                      <jats:italic>OPTN<\/jats:italic>\n                      ,\n                      <jats:italic>SYNJ1<\/jats:italic>\n                      , and\n                      <jats:italic>SQSTM1<\/jats:italic>\n                      . Other variants detected were in\n                      <jats:italic>TBK1<\/jats:italic>\n                      ,\n                      <jats:italic>PRNP<\/jats:italic>\n                      , and\n                      <jats:italic>ABCA7<\/jats:italic>\n                      \u2014genes that have been implicated in other neurodegenerative diseases. Eighteen patients had a positive family history, of whom two carried pathogenic\n                      <jats:italic>MAPT<\/jats:italic>\n                      variants, and one carried a likely pathogenic\n                      <jats:italic>GBA1<\/jats:italic>\n                      variant. None of the patients had expanded repeats in\n                      <jats:italic>C9orf72.<\/jats:italic>\n                      Furthermore, we found 16 different variants of uncertain significance in 21 PSP patients in\n                      <jats:italic>PSEN2<\/jats:italic>\n                      ,\n                      <jats:italic>ABCA7<\/jats:italic>\n                      ,\n                      <jats:italic>SMPD1<\/jats:italic>\n                      ,\n                      <jats:italic>MAPT<\/jats:italic>\n                      ,\n                      <jats:italic>ATP13A2<\/jats:italic>\n                      ,\n                      <jats:italic>OPTN<\/jats:italic>\n                      ,\n                      <jats:italic>SQSTM1<\/jats:italic>\n                      ,\n                      <jats:italic>CYLD<\/jats:italic>\n                      , and\n                      <jats:italic>BSN<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The genetic findings in our PSP cohorts appear to be somewhat distinct from those in Western populations, and also suggest an overlap of the genetic architecture between PSP and other neurodegenerative diseases. Further functional studies and validation in independent Asian cohorts will be useful for improving our understanding of PSP genetics and guiding genetic screening strategies in these populations. \u00a9 2024 International Parkinson and Movement Disorder Society.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mds.29932","type":"journal-article","created":{"date-parts":[[2024,8,16]],"date-time":"2024-08-16T04:55:37Z","timestamp":1723784137000},"page":"1829-1842","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Identification of Genetic Variants in Progressive Supranuclear Palsy in Southeast Asia"],"prefix":"10.1002","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8822-8496","authenticated-orcid":false,"given":"Adeline Su Lyn","family":"Ng","sequence":"first","affiliation":[{"name":"Department of Neurology National Neuroscience Institute  Singapore Singapore"},{"name":"Neuroscience and 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