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The central pore-forming protein TOM40 of the mitochondria is encoded by the translocase of outer mitochondrial membrane 40 homologue gene (\n                    <jats:italic>TOMM40<\/jats:italic>\n                    ). The highly variant\n                    <jats:italic>\u2018523\u2019<\/jats:italic>\n                    poly-T repeat is associated with age-related cognitive decline and age of onset in Alzheimer\u2019s disease, but whether it plays a role in modifying the risk or clinical course of PD it yet to be elucidated. The\n                    <jats:italic>TOMM40 \u2018523\u2019<\/jats:italic>\n                    allele length was determined in 634 people with PD and 422 healthy controls from an Australian cohort and the Parkinson\u2019s Progression Markers Initiative (PPMI) cohort, using polymerase chain reaction or whole genome sequencing analysis. Genotype and allele frequencies of\n                    <jats:italic>TOMM40 \u2018523\u2019<\/jats:italic>\n                    and\n                    <jats:italic>APOE<\/jats:italic>\n                    \u03b5 did not differ significantly between the cohorts. Analyses revealed\n                    <jats:italic>TOMM40 \u2018523\u2019<\/jats:italic>\n                    allele groups were not associated with disease risk, while considering\n                    <jats:italic>APOE<\/jats:italic>\n                    \u03b5 genotype. Regression analyses revealed the\n                    <jats:italic>TOMM40<\/jats:italic>\n                    S\/S genotype was associated with a significantly later age of symptom onset in the PPMI PD cohort, but not after correction for covariates, or in the Australian cohort. Whilst variation in the\n                    <jats:italic>TOMM40 \u2018523\u2019<\/jats:italic>\n                    polymorphism was not associated with PD risk, the possibility that it may be a modifying factor for age of symptom onset warrants further investigation in other PD populations.\n                  <\/jats:p>","DOI":"10.1038\/s41598-021-85510-0","type":"journal-article","created":{"date-parts":[[2021,3,18]],"date-time":"2021-03-18T12:47:41Z","timestamp":1616071661000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The TOMM40 \u2018523\u2019 polymorphism in disease risk and age of symptom onset in two independent cohorts of Parkinson\u2019s disease"],"prefix":"10.1038","volume":"11","author":[{"given":"Megan C.","family":"Bakeberg","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madison E.","family":"Hoes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anastazja M.","family":"Gorecki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frances","family":"Theunissen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abigail L.","family":"Pfaff","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jade E.","family":"Kenna","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kai","family":"Plunkett","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sulev","family":"K\u00f5ks","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. 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