{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,15]],"date-time":"2026-08-15T14:25:00Z","timestamp":1786803900360,"version":"build-2736575974"},"reference-count":55,"publisher":"American Medical Association (AMA)","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Neurol"],"published-print":{"date-parts":[[2025,8,1]]},"abstract":"<jats:sec id=\"ab-noi250038-4\"><jats:title>Importance<\/jats:title><jats:p>The impact of educational attainment (EA) on longitudinal tau accumulation remains largely underexplored.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-5\"><jats:title>Objective<\/jats:title><jats:p>To investigate the association of EA with tau accumulation in Alzheimer disease (AD).<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-6\"><jats:title>Design, Setting, and Participants<\/jats:title><jats:p>This cohort study used 3 independent samples: the Alzheimer\u2019s Disease Neuroimaging Initiative (ADNI; October 2015-July 2022, mean follow-up: 3.0 years), Anti-Amyloid Treatment in Asymptomatic Alzheimer\u2019s Disease study (A4; 2014-2022, mean follow-up: 4.7 years), and Greater-Bay-Area Healthy Aging Brain Study (GHABS; July 2021-August 2024, mean interval from plasma collection to tau positron emission tomography [PET]: 1.0 years). The ADNI and GHABS represent Northern American and Southern Chinese populations, respectively. A4 is a multicenter trial. Participants with amyloid \u03b2 (A\u03b2) and subsequent tau PET were included from ADNI, A4, and GHABS, and a subset had plasma phosphorylated tau (p-tau) 217 (p-tau217) and resting-state functional magnetic resonance imaging (RS-fMRI) data. Data were analyzed from July 2022 to January 2025.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-7\"><jats:title>Exposures<\/jats:title><jats:p>EA, A\u03b2-PET, tau-PET, plasma p-tau217, and RS-fMRI.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-8\"><jats:title>Main Outcomes and Measures<\/jats:title><jats:p>Participants were classified as high EA and low EA based on median years of EA. Longitudinal tau changes were compared across A\u03b2-PET positivity and EA groups. Interactions of EA status with A\u03b2 burden, entorhinal tau, and plasma p-tau217 on tau accumulation were investigated in A\u03b2-positive (A\u03b2+) individuals. Connectivity-associated tau spread was compared across different A\u03b2\/EA groups. Whether or not A\u03b2-targeting treatment attenuated tau accumulation in A\u03b2+ high-EA individuals was also evaluated.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-9\"><jats:title>Results<\/jats:title><jats:p>This study included 887 participants: 377 from ADNI (mean [SD] age, 73.3 [7.2] years; 191 female [50.7%]), 395 from A4 (mean [SD] age, 71.9 [4.8] years; 223 female [56.5%]), and 115 from GHABS (mean [SD] years, 66.0 [7.4] years; 76 female [66.1%]).  In the A\u03b2-negative group, high-EA individuals exhibited slower tau accumulation than low-EA individuals (right middle temporal gyrus: estimate = \u22120.002; 95% CI, \u22120.003 to \u22120.0002; <jats:italic>P<\/jats:italic> = .03). Conversely, higher EA in the A\u03b2+ group was correlated with accelerated tau accumulation (left middle temporal gyrus: estimate = 0.003; 95% CI, 0.0003-0.005; <jats:italic>P<\/jats:italic> = .03) and stronger A\u03b2-associated (left visual region: estimate = 0.38; 95% CI, 0.11-0.65; <jats:italic>P <\/jats:italic>= .006), entorhinal tau\u2013associated (left middle temporal gyrus: estimate = 0.35; 95% CI, 0.08-0.63; <jats:italic>P<\/jats:italic> = .01), and plasma p-tau217\u2013associated tau accumulation (left inferior temporal gyrus: estimate = 0.46; 95% CI, 0.02-0.90; <jats:italic>P <\/jats:italic>= .04), as well as increased connectivity-associated tau spread compared with lower EA (estimate = 0.33; 95% CI, 0.003-0.67; <jats:italic>P<\/jats:italic> = .048). A\u03b2-targeting treatment appeared to mitigate plasma p-tau217\u2013associated tau accumulation in patients with AD and higher EA (estimate\u2009=\u2009\u22120.52; 95% CI, \u22120.80 to \u22120.24; <jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u2009.001).<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi250038-10\"><jats:title>Conclusions and Relevance<\/jats:title><jats:p>Results of this cohort study suggest that higher EA was associated with faster tau accumulation and spread in A\u03b2+ individuals, highlighting the importance of A\u03b2 clearance in mitigating tau progression in patients with AD and higher EA.<\/jats:p><\/jats:sec>","DOI":"10.1001\/jamaneurol.2025.1801","type":"journal-article","created":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T11:00:40Z","timestamp":1751886040000},"page":"848","source":"Crossref","is-referenced-by-count":9,"title":["Higher Educational Attainment and Accelerated Tau Accumulation in Alzheimer Disease"],"prefix":"10.1001","volume":"82","author":[{"given":"Yue","family":"Cai","sequence":"first","affiliation":[{"name":"Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lili","family":"Fang","sequence":"additional","affiliation":[{"name":"Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Yang","sequence":"additional","affiliation":[{"name":"Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China"},{"name":"Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Zhou","sequence":"additional","affiliation":[{"name":"Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, 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