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Linear mixed effects models were used to examine the association between diffusion parameters and years from estimated symptom onset in\n C9orf72<\/jats:italic>\n ,\n \n MAPT<\/jats:styled-content>\n <\/jats:italic>\n , and\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n mutation carriers versus noncarriers. Post hoc analyses were performed on presymptomatic mutation carriers only, as well as left\u2013right asymmetry analyses on\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n mutation carriers versus noncarriers.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Diffusion changes in\n C9orf72<\/jats:italic>\n mutation carriers are present significantly earlier than both\n \n MAPT<\/jats:styled-content>\n <\/jats:italic>\n and\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n mutation carriers \u2013 characteristically in the posterior thalamic radiation and more posteriorly located tracts (e.g., splenium of the corpus callosum, posterior corona radiata), as early as 30 years before estimated symptom onset.\n \n MAPT<\/jats:styled-content>\n <\/jats:italic>\n mutation carriers showed early involvement of the uncinate fasciculus and cingulum, sparing the internal capsule, whereas involvement of the anterior and posterior internal capsule was found in\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n . Restricting analyses to presymptomatic mutation carriers only, similar \u2013 albeit less extensive \u2013 patterns were found: posteriorly located\n WM<\/jats:styled-content>\n tracts (e.g., posterior thalamic radiation, splenium of the corpus callosum, posterior corona radiata) in presymptomatic\n C9orf72<\/jats:italic>\n , the uncinate fasciculus in presymptomatic\n \n MAPT<\/jats:styled-content>\n <\/jats:italic>\n , and the internal capsule (anterior and posterior limbs) in presymptomatic\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n mutation carriers. In\n \n GRN<\/jats:styled-content>\n <\/jats:italic>\n , most tracts showed significant left\u2013right differences in one or more diffusion parameter, with the most consistent results being found in the\n UF<\/jats:styled-content>\n ,\n EC<\/jats:styled-content>\n ,\n RPIC<\/jats:styled-content>\n , and\n ALIC<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Interpretation<\/jats:title>\n \n This study demonstrates the presence of early and widespread\n WM<\/jats:styled-content>\n integrity loss in presymptomatic\n FTD<\/jats:styled-content>\n , and suggests a clear genotypic \u201cfingerprint.\u201d Our findings corroborate the notion of\n FTD<\/jats:styled-content>\n as a network\u2010based disease, where changes in connectivity are some of the earliest detectable features, and identify diffusion tensor imaging as a potential neuroimaging biomarker for disease\u2010tracking and \u2010staging in presymptomatic to early\u2010stage familial\n FTD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/acn3.601","type":"journal-article","created":{"date-parts":[[2018,7,11]],"date-time":"2018-07-11T03:37:54Z","timestamp":1531280274000},"page":"1025-1036","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":60,"title":["Presymptomatic white matter integrity loss in familial frontotemporal dementia in the\n GENFI<\/scp>\n cohort: A cross\u2010sectional diffusion tensor imaging study"],"prefix":"10.1002","volume":"5","author":[{"given":"Lize C.","family":"Jiskoot","sequence":"first","affiliation":[{"name":"Department of Neurology Erasmus Medical Center Rotterdam the Netherlands"},{"name":"Dementia Research Center University College London London United Kingdom"},{"name":"Department of Radiology Leiden University Medical Center Leiden the 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