{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T11:41:19Z","timestamp":1765280479608,"version":"build-2065373602"},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,2,24]],"date-time":"2025-02-24T00:00:00Z","timestamp":1740355200000},"content-version":"vor","delay-in-days":54,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01AG037639","R01AG027161","P50AG033514"],"award-info":[{"award-number":["R01AG037639","R01AG027161","P50AG033514"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alz &amp; Dem Diag Ass &amp; Dis Mo"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>INTRODUCTION<\/jats:title><jats:p>This study examined the association of longitudinal atrophy with baseline cerebrospinal fluid (CSF) amyloid beta (A\u03b2, A) and phosphorylated tau (p\u2010tau, T) biomarkers (A\u03b242\/40, p\u2010tau181) in 406 cognitively unimpaired (CU) individuals (6.670 years of follow\u2010up on average, up to 13 imaging visits) to assess whether A+ is associated with Alzheimer's disease\u2013like atrophy and whether this depends on p\u2010tau181 levels.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>An A\u2010T\u2010 CU group free from abnormal neurodegeneration (N) was identified using a robust normative approach and used to model normal age\u2010related atrophy via <jats:italic>z<\/jats:italic>\u2010scoring. Linear mixed\u2010effects models tested differences in longitudinal atrophy between A+ and A\u2010T\u2010N\u2010 individuals and between A\/T subgroups.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>A+ was associated with worse atrophy within and beyond the medial temporal lobe, even at low levels of p\u2010tau181.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>Neurodegeneration likely begins soon after the onset of abnormal A\u03b2 pathology. Clinical intervention at the earliest signs of A\u03b2 pathology may be needed to mitigate further neurodegeneration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>An A\u2010T\u2010N\u2010 control group was identified using a robust normative approach<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>A+ was associated with accelerated atrophy in cognitively unimpaired individuals<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Atrophy was observed even at low p\u2010tau181 levels<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/dad2.70089","type":"journal-article","created":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T13:52:10Z","timestamp":1740577930000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Amyloid is associated with accelerated atrophy in cognitively unimpaired 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