{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T04:58:44Z","timestamp":1771045124805,"version":"3.50.1"},"reference-count":537,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2023,3,9]],"date-time":"2023-03-09T00:00:00Z","timestamp":1678320000000},"content-version":"vor","delay-in-days":67,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>\u03b1-Synuclein is a pleiotropic protein underlying a group of progressive neurodegenerative diseases, including Parkinson\u2019s disease and dementia with Lewy bodies. Together, these are known as synucleinopathies. Like all neurological diseases, understanding of disease mechanisms is hampered by the lack of access to biopsy tissues, precluding a real-time view of disease progression in the human body. This has driven researchers to devise various experimental models ranging from yeast to flies to human brain organoids, aiming to recapitulate aspects of synucleinopathies. Studies of these models have uncovered numerous genetic modifiers of \u03b1-synuclein, most of which are evolutionarily conserved. This review discusses what we have learned about disease mechanisms from these modifiers, and ways in which the study of modifiers have supported ongoing efforts to engineer disease-modifying interventions for synucleinopathies.<\/jats:p>","DOI":"10.1093\/oons\/kvad001","type":"journal-article","created":{"date-parts":[[2023,3,9]],"date-time":"2023-03-09T19:15:11Z","timestamp":1678389311000},"source":"Crossref","is-referenced-by-count":4,"title":["Genetic modifiers of synucleinopathies\u2014lessons from experimental models"],"prefix":"10.1093","volume":"2","author":[{"given":"Rachel Min Qi","family":"Lee","sequence":"first","affiliation":[{"name":"Temasek Life Sciences Laboratory , 1 Research Link, Singapore, 117604, Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tong-Wey","family":"Koh","sequence":"additional","affiliation":[{"name":"Temasek Life Sciences Laboratory , 1 Research Link, Singapore, 117604, Singapore"},{"name":"National University of Singapore Department of Biological Sciences, , Block S3 #05-01, 16 Science Drive 4, Singapore, 117558, Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2023,3,9]]},"reference":[{"key":"2024031905564650200_ref1","doi-asserted-by":"crossref","first-page":"13","DOI":"10.1038\/nrneurol.2012.242","article-title":"100 years of Lewy pathology","volume":"9","author":"Goedert","year":"2013","journal-title":"Nat Rev Neurol"},{"key":"2024031905564650200_ref2","doi-asserted-by":"crossref","first-page":"839","DOI":"10.1038\/42166","article-title":"\u03b1-Synuclein in Lewy bodies","volume":"388","author":"Spillantini","year":"1997","journal-title":"Nature"},{"key":"2024031905564650200_ref3","doi-asserted-by":"crossref","first-page":"11282","DOI":"10.1073\/pnas.90.23.11282","article-title":"Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer 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