{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T06:58:09Z","timestamp":1792825089850,"version":"4.5.0"},"posted":{"date-parts":[[2026,1,26]]},"group-title":"Neurology","reference-count":62,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,1,26]],"date-time":"2026-01-26T00:00:00Z","timestamp":1769385600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,1,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>Early-onset Alzheimer\u2019s disease (EOAD) and Late-onset AD (LOAD) differ in clinical presentations and rates of progression. We aimed to compare baseline and longitudinal tau PET burden, and their relationship with clinical variables in amyloid-PET positive, cognitively impaired participants from the Longitudinal Early-Onset Alzheimer\u2019s Disease Study (EOAD; n=390) and Alzheimer\u2019s Disease Neuroimaging Initiative (LOAD; n=211). Patients with EOAD showed higher baseline tau PET retention, broader neuroanatomical involvement and faster accumulation rates over time compared to LOAD, after adjusting for amyloid load and clinical stage. Tau PET showed stronger correlations with baseline amyloid burden and clinical measures of global cognition and function in EOAD than LOAD. We conclude that earlier age of onset in AD is linked to a more aggressive tauopathy, which in turn is a primary driver of clinical decline. These findings suggest that optimal therapeutic targets and strategies may differ between EOAD and LOAD.<\/jats:p>\n                <jats:sec>\n                  <jats:title>One Sentence Summary<\/jats:title>\n                  <jats:p>Younger patients with Alzheimer\u2019s disease show more aggressive tau spread, suggesting age of onset defines distinct disease pathways with key clinical implications.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.01.25.26344738","type":"posted-content","created":{"date-parts":[[2026,1,26]],"date-time":"2026-01-26T23:30:17Z","timestamp":1769470217000},"source":"Crossref","is-referenced-by-count":3,"title":["Distinct Tau PET Dynamics in Early vs. Late Age-of-Onset Alzheimer\u2019s disease"],"prefix":"10.64898","author":[{"given":"Konstantinos","family":"Chiotis","sequence":"first","affiliation":[{"name":"Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco; San Francisco, California 94143, USA"},{"name":"Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet; Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganna","family":"Blazhenets","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco; San Francisco, California 94143, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David N.","family":"Soleimani-Meigooni","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco; San Francisco, California 94143, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul S.","family":"Aisen","sequence":"additional","affiliation":[{"name":"Alzheimer\u2019s Therapeutic Research Institute, Keck School of Medicine, University of Southern California; San Diego, California 92121, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alinda","family":"Amuiri","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco; 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