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Hillblom Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001167","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010292","name":"Banner Alzheimer\u2019s Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010292","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>In comparison with late\u2010onset Alzheimer's disease (LOAD, onset, &gt;65 years), early\u2010age\u2010of\u2010onset Alzheimer's disease (EOAD, onset, &lt;65 years) more often presents with language, visuospatial, and\/or executive impairment, often occurring earlier than a progressive memory deficit. The logopenic variant of primary progressive aphasia (lv\u2010PPA) and posterior cortical atrophy (PCA) have recently been described as possible atypical variants of EOAD. Lv\u2010PPA is characterized by isolated language deficit, whereas PCA is characterized by predominant visuospatial deficits. Severe hemispheric gray matter (GM) atrophy associated with EOAD, lv\u2010PPA, and PCA has been described, but regional patterns of white matter (WM) damage are still poorly understood.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Using structural magnetic resonance imaging and voxel\u2010based morphometry, we investigated WM damage in patients with EOAD (n = 16), PCA (n = 13), lv\u2010PPA (n = 10), and LOAD (n = 14) at presentation and 72 age\u2010matched control subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In patients with EOAD, PCA, and lv\u2010PPA, WM atrophy was centered on the lateral temporal and parietal regions, including the cingulum and posterior corpus callosum. Compared with control subjects, patients with lv\u2010PPA showed more severe left parietal damage, and patients with PCA showed more severe occipital atrophy. Moreover, patients with EOAD had greater cingulum atrophy compared with those with LOAD. LOAD showed WM damage in the medial temporal regions and less extensive hemispheric involvement.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Patterns of WM damage in EOAD, lv\u2010PPA, and PCA are consistent with the clinical syndromes and GM atrophy patterns. WM injury in AD atypical variants may contribute to symptoms and disease pathogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.jalz.2012.04.010","type":"journal-article","created":{"date-parts":[[2012,9,25]],"date-time":"2012-09-25T18:07:20Z","timestamp":1348596440000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":67,"title":["White matter atrophy in Alzheimer's disease variants"],"prefix":"10.1002","volume":"8","author":[{"given":"Raffaella","family":"Migliaccio","sequence":"first","affiliation":[{"name":"Memory and Aging Center Department of Neurology University of California at San Francisco San Francisco CA USA"},{"name":"Inserm-UPMC UMRS 975, CR-ICM Centre de Recherche de l'Institut du Cerveau et de la Moelle Epini\u00e8re H\u00f4pital Piti\u00e9-Salp\u00eatri\u00e8re Paris France"},{"name":"Department of Psychology Catholic University Milan Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federica","family":"Agosta","sequence":"additional","affiliation":[{"name":"Neuroimaging Research Unit Institute of Experimental Neurology Division of Neuroscience San Raffaele Scientific Institute Vita-Salute San Raffaele University Milan Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine L.","family":"Possin","sequence":"additional","affiliation":[{"name":"Memory and Aging Center Department of Neurology University of California at San Francisco San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gil D.","family":"Rabinovici","sequence":"additional","affiliation":[{"name":"Memory and Aging Center Department of Neurology University of California at San Francisco San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce L.","family":"Miller","sequence":"additional","affiliation":[{"name":"Memory and Aging Center Department of Neurology University of California at San Francisco San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Luisa","family":"Gorno-Tempini","sequence":"additional","affiliation":[{"name":"Memory and Aging Center Department of Neurology University of California at San Francisco San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,10]]},"reference":[{"key":"e_1_2_10_2_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0b013e3181c0d427"},{"key":"e_1_2_10_3_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1988.00520310107024"},{"key":"e_1_2_10_4_2","doi-asserted-by":"publisher","DOI":"10.1212\/01.wnl.0000320506.79811.da"},{"key":"e_1_2_10_5_2","doi-asserted-by":"publisher","DOI":"10.1159\/000058331"},{"key":"e_1_2_10_6_2","doi-asserted-by":"publisher","DOI":"10.1212\/01.WNL.0000140289.18472.15"},{"key":"e_1_2_10_7_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/123.3.484"},{"key":"e_1_2_10_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.74.11.1521"},{"key":"e_1_2_10_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00415-005-0594-5"},{"key":"e_1_2_10_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2006.05.026"},{"key":"e_1_2_10_11_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0b013e31821103e6"},{"key":"e_1_2_10_12_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.59.2.243"},{"key":"e_1_2_10_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2010.09.021"},{"key":"e_1_2_10_14_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awr099"},{"key":"e_1_2_10_15_2","unstructured":"FAgosta EScola ECanu AMarcone GMagnani LSarro et al.White matter damage in frontotemporal lobar degeneration spectrum. 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