{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T20:28:50Z","timestamp":1790800130138,"version":"4.1.0"},"reference-count":64,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T00:00:00Z","timestamp":1724803200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100008931","name":"California Earthquake Authority","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008931","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":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>INTRODUCTION<\/jats:title><jats:p>Typical Alzheimer's disease (AD) and limbic\u2010predominant age\u2010related TAR DNA\u2010binding protein 43 (TDP\u201043) encephalopathy (LATE) are two neurodegenerative diseases that present with a similar initial amnestic clinical phenotype but are associated with distinct proteinopathies.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>We investigated white matter (WM) fiber bundle alterations, using fixel\u2010based analysis, a state\u2010of\u2010the\u2010art diffusion magnetic resonance imaging model, in early AD, presumed LATE, and controls. We also investigated regional cortical atrophy.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>Both amnestic AD and presumed LATE patients exhibited WM alterations in tracts of the temporal and limbic lobes and in callosal fibers connecting superior frontal gyri. In addition, presumed LATE patients showed alterations in callosal fibers connecting the middle frontal gyri and in the cerebello\u2013thalamo\u2013cortical tract. Cortical thickness was reduced in regions connected by the most altered tracts.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>These findings, the first to describe WM fiber bundle alterations in presumed LATE, are consistent with results on cortical atrophy and with the staging system of tau or TDP\u201043 accumulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Fixel\u2010based analysis revealed white matter (WM) fiber bundle alterations in presumed limbic\u2010predominant age\u2010related TAR DNA\u2010binding protein 43 encephalopathy (LATE) patients identified by isolated episodic\/limbic amnesia, the absence of positive Alzheimer's disease (AD) biomarkers, and no other neurological diagnosis after 2 years of follow\u2010up.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Presumed LATE and amnestic AD shared similar patterns of WM alterations in fiber bundles of the limbic and temporal lobes, in congruence with their similar limbic cognitive phenotype.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Presumed LATE differed from AD by the alteration of the callosal fibers connecting the middle frontal gyri and of the cerebello\u2013thalamo\u2013cortical tract.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>WM fiber bundle alterations were consistent with results on regional cortical atrophy.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The different anatomical patterns of WM degeneration could provide information on the propagation pathways of distinct proteinopathies.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.14156","type":"journal-article","created":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T04:46:37Z","timestamp":1724820397000},"page":"6922-6934","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["How fiber bundle alterations differ in presumed LATE and amnestic Alzheimer's disease"],"prefix":"10.1002","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-6168-8964","authenticated-orcid":false,"given":"Aur\u00e9lie","family":"Lebrun","sequence":"first","affiliation":[{"name":"Universit\u00e9 Paris\u2010Saclay UNIACT, NeuroSpin, CEA  Gif\u2010sur\u2010Yvette France"},{"name":"Universit\u00e9 Paris\u2010Saclay, BioMaps Service Hospitalier Fr\u00e9d\u00e9ric Joliot, CEA, CNRS, Inserm  Orsay France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yann","family":"Leprince","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris\u2010Saclay UNIACT, NeuroSpin, CEA  Gif\u2010sur\u2010Yvette France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julien","family":"Lagarde","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris\u2010Saclay, BioMaps Service Hospitalier Fr\u00e9d\u00e9ric Joliot, CEA, CNRS, Inserm  Orsay France"},{"name":"Department of Neurology of Memory and Language GHU Paris Psychiatrie &amp; Neurosciences H\u00f4pital Sainte\u2010Anne  Paris France"},{"name":"Universit\u00e9 Paris\u2010Cit\u00e9  Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pauline","family":"Olivieri","sequence":"additional","affiliation":[{"name":"Department of Neurology of Memory and Language GHU Paris Psychiatrie &amp; Neurosciences H\u00f4pital Sainte\u2010Anne  Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Moussion","sequence":"additional","affiliation":[{"name":"Department of Neurology of Memory and Language GHU Paris Psychiatrie &amp; Neurosciences H\u00f4pital Sainte\u2010Anne  Paris France"},{"name":"Centre d'Evaluation Troubles Psychiques et Vieillissement GHU Paris Psychiatrie &amp; Neurosciences H\u00f4pital Sainte Anne  Paris 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