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This work tests whether longitudinal tau-PET accumulation is clinically relevant by relating higher accumulation to atrophy and cognitive decline. Method: 333 BioFINDER-2 participants underwent Aβ-PET and CSF Aβ42/Aβ40 screening; tau-PET ROC was estimated with linear mixed-effects models across composite ROIs. Result: 16% were tau-accumulators, showing older age and different CSF profiles and greater baseline and non-Braak I–IV accumulation; baseline cognition was worse without a different longitudinal decline.",{"@graph":69,"@context":123},[70,84,106],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/longitudinal-tau-pet-accumulation-and-downstream-effects-in-amyloid-beta-negative-cognitively-unimpaired-individuals-podium-presentation/455968/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/longitudinal-tau-pet-accumulation-and-downstream-effects-in-amyloid-beta-negative-cognitively-unimpaired-individuals-podium-presentation/455968.png","ImageObject",300,407,{"name":92,"@type":93},"Fahsai","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What population was studied and how were participants selected?","Question",{"text":113,"@type":114},"The study included 333 cognitively unimpaired BioFINDER-2 participants who were negative for both global [18F]flutemetamol Aβ-PET and CSF Aβ42/Aβ40.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How were tau-accumulators defined?",{"text":118,"@type":114},"Individuals were classified as “tauaccumulators” versus “non-accumulators” using the mean plus standard deviation of Braak I-IV tau-PET ROC in young controls (20–40 years).",{"name":120,"@type":111,"acceptedAnswer":121},"What downstream effects were assessed and what was the main conclusion?",{"text":122,"@type":114},"Downstream effects included atrophy and cognitive performance, using measures such as entorhinal cortex/BA35 thickness and cognition composites. Aβ-negative CU individuals showed longitudinal neocortical tau accumulation, associated with a tau-specific CSF biomarker and focal atrophy, but without translated changes in cognitive decline.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},455968,1790789745,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":19,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":52,"preview_page_count":4},549768702563,"https://ap-avatar.wpscdn.com/avatar/8000c4aa63b76e948b?x-image-process=image/resize,m_fixed,w_180,h_180&k=1786536092046926083","DOI: 10. 1002/alz70856_104826  \nBIOMARKERS  \nPODIUM PRESENTATION  \nNEUROIMAGING  \nLongitudinal tau-PET accumulation and downstream effects in amyloid-beta negative cognitively unimpaired individuals  \nAnika Wuestefeld1  Nicola Spotorno 1  Alexa Pichet Binette2, 3, 4   \nNiklas Mattsson-Carlgren5, 6, 7  Rik Ossenkoppele8  Sebastian Palmqvist 1, 6  Ruben Smith5, 6  Erik Stomrud 1, 6  Olof Strandberg 1  Danielle van Westen9, 10 Oskar Hansson 1  Laura E. M. Wisse 11  \n1 Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden  \n2 Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, MOntreal, QC, Canada  \n3 Department of Physiology and Pharmacology, Université de Montréal, Montréal, QC, Canada  \n4 Centre de recherche de l’institut universitaire de gériatrie de Montréal (CRIUGM), Montréal, QC, Canada  \n5 Clinical Memory Research Unit, Lund University, Malmö, Skåne, Sweden  \n6 Memory Clinic, Skåne University Hospital, Malmö, Skåne, Sweden  \n7Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden  \n8 Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden  \n9 Imaging and Function, Skåne University Hospital, Lund, Sweden  \n10 Department of Diagnostic Radiology, Clinical Sciences, Lund University, Lund, Sweden  \n11 Diagnostic Radiology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden  \nCorrespondence  \nAnika Wuestefeld, Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.  \nEmail: [anika.wuestefeld@gmail.com](anika.wuestefeld@gmail.com)  \nAbstract  \nBackground: Previous studies, including ours (Wuestefeld et al., Brain, 2023), showed tau positron emission tomography (PET) uptake in medial temporal and neocortical regions of amyloid-beta (Aβ)-negative cognitively unimpaired (CU) individuals, associated with neurodegeneration and worse memory performance. To further understand if tau-PET uptake is clinically relevant in this population, we characterized Aβ-negative CU individuals with higher longitudinal tau-PET accumulation and its associations with atrophy and cognitive decline.  \nMethod: We included 333 CU BioFINDER-2 participants, negative for both global [18F]flutemetamol Aβ-PET and cerebrospinal fluid (CSF) Aβ42/Aβ40 (age=63.8, 55% female, 2.28± 1. 36 years follow-up). Using linear mixed-effects models, we calculated the rate of change (ROC) in [18F]RO948 tau-PET SUVR in composite regions of interest (ROI), recapitulating the Braak stages. Individuals were classified as “tauaccumulators”vs.“non-accumulators”based on the mean+standard deviation of Braak I-IV tau-PET ROC in young controls (20-40 years, n = 29; Figure 1A). Tau-PET ROC and thickness of the entorhinal cortex, Brodmann area (BA)35 and neocortical AD-regions (precuneus/posterior cingulate, lateral occipital, superior frontal) were extracted. Group differences and associations with CSF AD biomarkers, delayed word-list recall, and modified Preclinical Alzheimer Cognitive Composite were tested.  \nResult: 16% of individuals were identified as tau-accumulators. They were older, had lower levelsofAβ as indicated by a higher CSFAβ42/40ratio(no difference on Aβ-PET)  \nand numerically higher CSF MTBR-tau243/Aβ40 (not significant, note missingness; Figure 1B+C). Tau-accumulators showed significantly greater tau-PET at baseline and accumulation in regions not included in Braak I-IV (all p \u003C0.001). Additionally, we  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2025 The Alzheimer’s Association. Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association.  \nAlzheimer’s Dement. 2025;21(Suppl. 2):e104826.  \n[https://doi.org/10.1002/alz70856_104826](https://doi.org/10.1002/a","cbCaifmKZM229aXr","https://ap.wps.com/l/cbCaifmKZM229aXr","pdf",3396000,"English","# Background\n# Method\n# Results\n# Conclusion","[{\"question\":\"What population was studied and how were participants selected?\",\"answer\":\"The study included 333 cognitively unimpaired BioFINDER-2 participants who were negative for both global [18F]flutemetamol Aβ-PET and CSF Aβ42/Aβ40.\"},{\"question\":\"How were tau-accumulators defined?\",\"answer\":\"Individuals were classified as “tauaccumulators” versus “non-accumulators” using the mean plus standard deviation of Braak I-IV tau-PET ROC in young controls (20–40 years).\"},{\"question\":\"What downstream effects were assessed and what was the main conclusion?\",\"answer\":\"Downstream effects included atrophy and cognitive performance, using measures such as entorhinal cortex/BA35 thickness and cognition composites. Aβ-negative CU individuals showed longitudinal neocortical tau accumulation, associated with a tau-specific CSF biomarker and focal atrophy, but without translated changes in cognitive decline.\"}]","Longitudinal tau-PET accumulation and downstream effects in amyloid-beta negative cognitively unimpaired individuals - PODIUM PRESENTATION | PDF",1790744807]