{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T17:51:05Z","timestamp":1791395465936,"version":"4.3.3"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T00:00:00Z","timestamp":1782691200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T00:00:00Z","timestamp":1782691200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100000272","name":"National Institute for Health and Care Research","doi-asserted-by":"publisher","award":["CL\u20102023\u201012\u2010003"],"award-info":[{"award-number":["CL\u20102023\u201012\u2010003"]}],"id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alz &amp;amp; Dem Diag Ass &amp;amp; Dis Mo"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>Anti\u2010amyloid therapies (AATs) for Alzheimer's disease (AD) demonstrate modest benefit in trials, but real\u2010world eligibility remains uncertain. Requirements including biomarker confirmation and safety exclusions may limit access.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      Using the Brains for Dementia Research cohort, we linked longitudinal cognitive data with\n                      <jats:italic>post mortem<\/jats:italic>\n                      neuropathology to estimate trial\u2010like AAT eligibility. Early stage was defined using harmonized cognitive thresholds. AD pathology required Thal amyloid phase \u22653 and Braak stage \u2265IV. Exclusions were applied hierarchically: (1) vascular neuropathology, (2) anticoagulant use, and (3)\n                      <jats:italic>apolipoprotein E<\/jats:italic>\n                      (\n                      <jats:italic>APOE<\/jats:italic>\n                      )\u00a0\u03b54\/\u03b54\u00a0homozygosity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      Of 1230 participants, 945 had sufficient data; 232 had early, pathology\u2010confirmed AD. Vascular pathology excluded 70.7%, anticoagulant use 19.1%, and\n                      <jats:italic>APOE<\/jats:italic>\n                      \u03b54\/\u03b54 homozygosity 3.6% of remaining cases. Overall, 53 individuals (4.3% of those screened) were eligible. Eligibility declined with age and was driven primarily by vascular comorbidity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>Using a conservative pathology\u2010anchored framework, only a small proportion of this older brain\u2010donor cohort met trial\u2010like eligibility criteria.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/dad2.70400","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T03:29:55Z","timestamp":1782790195000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Anti\u2010amyloid therapy eligibility in a longitudinal brain\u2010donor cohort with\n                    <i>post mortem<\/i>\n                    confirmation"],"prefix":"10.1002","volume":"18","author":[{"given":"Monjurul","family":"Haque","sequence":"first","affiliation":[{"name":"Department of Neurology Nottingham University Hospitals NHS Trust  Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keeley J.","family":"Brookes","sequence":"additional","affiliation":[{"name":"Biosciences Nottingham Trent University  Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-5333-370X","authenticated-orcid":false,"given":"Beili","family":"Shao","sequence":"additional","affiliation":[{"name":"Department of Neurology Nottingham University Hospitals NHS Trust  Nottingham UK"},{"name":"Academic Neurology, Academic Unit of Mental Health and Clinical Neurosciences, School of Medicine University of Nottingham  Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,29]]},"reference":[{"key":"e_1_2_10_2_1","unstructured":"Alzheimer's Society.The economic impact of dementia module 1: annual costs of dementia.2024."},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2023.13239"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2212948"},{"key":"e_1_2_10_5_1","unstructured":"AndersonR KnappM WittenbergR HandelsR SchottJM Modelling of disease\u2010modifying therapies in Alzheimer's disease. 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