{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T17:01:49Z","timestamp":1791478909905,"version":"4.3.4"},"reference-count":75,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T00:00:00Z","timestamp":1761091200000},"content-version":"vor","delay-in-days":21,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000957","name":"Alzheimer's Association","doi-asserted-by":"publisher","award":["AARG\u201022\u2010973496"],"award-info":[{"award-number":["AARG\u201022\u2010973496"]}],"id":[{"id":"10.13039\/100000957","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":[[2025,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>\n                      With anti\u2010amyloid beta (A\u03b2) therapies approved for Alzheimer's disease (AD), surrogate biomarkers are needed to monitor clinical treatment efficacy. Therefore, we systematically compared longitudinal changes in A\/T\/N biomarkers (amyloid\u2010positron emission tomography [PET], tau\u2010PET, plasma phosphorylated tau at threonine 217 [p\u2010tau\n                      <jats:sub>217<\/jats:sub>\n                      ], and magnetic resonance imaging) for tracking cognitive changes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      We analyzed longitudinal biomarker and cognitive change rates from the Alzheimer's Disease Neuroimaging Initiative (\n                      <jats:italic>N\u00a0<\/jats:italic>\n                      =\u00a0141) and Anti\u2010Amyloid Treatment in Asymptomatic Alzheimer's (A4) and Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) (\n                      <jats:italic>N<\/jats:italic>\n                      \u00a0=\u00a0151), estimated using linear mixed models. Using linear models, we tested biomarker changes as predictors of cognitive changes, comparing predictive strengths across biomarkers using bootstrapping.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Tau\u2010PET, plasma p\u2010tau217, and cortical thickness changes accurately tracked change rates in Mini\u2010Mental State Examination, Alzheimer's Disease Assessment Scale\u2010Cognitive Subscale 13\u2010item version, Clinical Dementia Rating\u2010Sum of Boxes, and Preclinial Alzheimer Cognitive Composite scores. In contrast, amyloid\u2010PET change rates were not linked to cognitive changes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>\n                      Plasma p\u2010tau\n                      <jats:sub>217<\/jats:sub>\n                      offers a cost\u2010effective AD\u2010specific alternative to tau\u2010PET and could potentially be implemented for monitoring cognitive changes in AD trials, while amyloid\u2010PET lacks utility. Cortical thickness changes accurately track cognitive changes but may be confounded by pseudo\u2010atrophy in anti\u2010A\u03b2 treatments.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Longitudinal changes in tau\u2010PET, plasma p\u2010tau\n                            <jats:sub>217<\/jats:sub>\n                            , cortical thickness \u2013 but not amyloid\u2010PET \u2013 effectively track cognitive decline.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Cortical thickness may be confounded by pseudo\u2010atrophy in anti\u2010A\u03b2 trials.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Plasma p\u2010tau\n                            <jats:sub>217<\/jats:sub>\n                            is a robust and cost\u2010effective alternative to tau\u2010PET as an AD\u2010specific surrogate biomarker for monitoring cognitive changes.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.70783","type":"journal-article","created":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T04:19:33Z","timestamp":1761193173000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["A systematic comparison of ATN biomarkers for monitoring longitudinal cognitive changes in Alzheimer's 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