{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T09:14:26Z","timestamp":1783415666655,"version":"3.54.6"},"reference-count":63,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T00:00:00Z","timestamp":1780099200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T00:00:00Z","timestamp":1780099200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/501100010767","name":"Innovative Medicines Initiative","doi-asserted-by":"publisher","award":["2 Joint Undertaking, grant agreement 101034344"],"award-info":[{"award-number":["2 Joint Undertaking, grant agreement 101034344"]}],"id":[{"id":"10.13039\/501100010767","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010767","name":"Innovative Medicines Initiative","doi-asserted-by":"publisher","award":["2 Joint Undertaking, grant agreement 115952"],"award-info":[{"award-number":["2 Joint Undertaking, grant agreement 115952"]}],"id":[{"id":"10.13039\/501100010767","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Identifying factors associated with early progression of cortical amyloid deposition is crucial for understanding Alzheimer's disease (AD) pathophysiology, yet these remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      To investigate the associations of AD cerebrospinal fluid (CSF) biomarkers with early longitudinal amyloid deposition on positron emission tomography (PET), and the impact of\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriership.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We selected cognitively unimpaired participants with baseline data on CSF amyloid and p-tau181,\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriership, and \u2265 2 consecutive amyloid PET assessments from the AMYPAD-PNHS cohort. Linear mixed models were used to investigate the associations of combinations of amyloid abnormality (A+) and tau abnormality (T+) in CSF (A+T+, A+T-, A-T+, A-T-), without and with stratification for\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriership, with longitudinal global cortical amyloid deposition on PET, measured in Centiloids.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We included 329 individuals (mean age 63.5 [SD 6.1], 58% female, 49%\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriers). Longitudinally, CSF profiles with abnormal amyloid levels (A+T+, A+T-) showed greater increases in cortical amyloid deposition than profiles with normal amyloid levels (A-T+, A-T-), irrespective of CSF tau abnormality (all p\u2009&lt;\u20090.001). Only for CSF profiles with normal amyloid levels, longitudinal amyloid deposition depended on\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriership, with both A-T+\u2009and A-T- showing increased deposition among\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriers (carriers versus non-carriers: A-T+\u2009p\u2009=\u20090.006, A-T- p\u2009=\u20090.016).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      In cognitively unimpaired individuals, longitudinal increase in cortical amyloid deposition was mainly associated with abnormal baseline CSF amyloid rather than tau.\n                      <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                      \u03b54 carriership was associated with increased longitudinal cortical amyloid deposition only in individuals with normal baseline CSF amyloid. These findings inform early AD pathological progression and trial design.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877261453099","type":"journal-article","created":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T08:59:31Z","timestamp":1780131571000},"page":"875-885","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Longitudinal amyloid PET changes by cerebrospinal fluid amyloid and tau profiles in individuals with normal cognition: Role of\n                    <i>APOE<\/i>\n                    \u03b54"],"prefix":"10.1177","volume":"112","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1980-5095","authenticated-orcid":false,"given":"Marianna","family":"Rizzo","sequence":"first","affiliation":[{"name":"Maastricht University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5201-8080","authenticated-orcid":false,"given":"Julie E.","family":"Oomens","sequence":"additional","affiliation":[{"name":"Maastricht University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9081-1496","authenticated-orcid":false,"given":"Willemijn J.","family":"Jansen","sequence":"additional","affiliation":[{"name":"Maastricht University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8008-9727","authenticated-orcid":false,"given":"Pieter Jelle","family":"Visser","sequence":"additional","affiliation":[{"name":"Maastricht University"},{"name":"Amsterdam Neuroscience"},{"name":"Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc"},{"name":"Karolinska Institutet"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2045-9818","authenticated-orcid":false,"given":"Stephanie J. B.","family":"Vos","sequence":"additional","affiliation":[{"name":"Maastricht University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"on behalf of the AMYPAD consortium","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,5,30]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S2468-2667(21)00249-8"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000010596"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/aww015"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.aaz2387"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2015.1285"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.24719"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2021.4654"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1002\/alz.13859"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2018.02.018"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2023.2338"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2020.05.012"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awy103"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.21843"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1002\/alz.12069"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13195-023-01332-4"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.trci.2016.02.003"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1136\/bmjopen-2017-021017"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13195-018-0406-7"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13195-017-0314-2"},{"key":"e_1_3_3_21_2","first-page":"100","article-title":"FACEHBI: a prospective study of risk factors, biomarkers and cognition in a cohort of individuals with subjective cognitive decline. 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