{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:33:02Z","timestamp":1777397582417,"version":"3.51.4"},"reference-count":88,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2025,9,1]],"date-time":"2025-09-01T00:00:00Z","timestamp":1756684800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01-AG068990"],"award-info":[{"award-number":["R01-AG068990"]}],"id":[{"id":"10.13039\/100000049","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":[[2025,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Plasma p-tau181 is a promising diagnostic marker of Alzheimer's disease (AD) pathology, reflecting amyloid accumulation, tau deposition, and downstream neurodegeneration that leads to cognitive impairment. However, the specificity of plasma p-tau181 to AD-related tau pathology remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To assess whether plasma p-tau181 is differentially associated with volumetric changes in distinct structures of the hippocampal formation and whether these structures mediate the relationship between plasma p-tau181 and cognition across the AD continuum.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>213 participants with normal cognition (N\u2009=\u200957), mild cognitive impairment (N\u2009=\u2009109), and AD (N\u2009=\u200947) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) were included for cross-sectional analyses of hippocampal formation volume that was quantified using the Automatic Segmentation of Hippocampal Subfields (ASHS) software. A subset (n\u2009=\u200989) was evaluated for one-year longitudinal changes in hippocampal formation volume.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Higher plasma p-tau181 levels (pg\/mL) were associated with decreased volumes in the CA1 and dentate gyrus, bilaterally, and right entorhinal cortex (\n                      <jats:italic>ps<\/jats:italic>\n                      \u2009&lt;\u20090.05). Additionally, volumes of these subfields partially mediated the relationship between plasma p-tau181 and ADNI memory and executive function composite scores. Baseline plasma p-tau181, however, did not predict longitudinal atrophy of hippocampal formation structures across diagnostic groups.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Plasma p-tau181 is differentially associated with regions of the hippocampal formation that are closely related to both age- and AD-related neurodegeneration. Elevated plasma p-tau181 levels may reflect tau pathology, and volumetric changes in CA1 and DG may mediate the detrimental effect of tau pathology on cognition.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251361354","type":"journal-article","created":{"date-parts":[[2025,7,28]],"date-time":"2025-07-28T06:50:51Z","timestamp":1753685451000},"page":"561-574","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Distinctive volumetric associations between plasma p-tau181 and hippocampal formation structures across the Alzheimer's disease continuum"],"prefix":"10.1177","volume":"107","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-2163-2164","authenticated-orcid":false,"given":"Adea","family":"Rich","sequence":"first","affiliation":[{"name":"Department of Epidemiology, Brown University School of Public Health, Providence, RI, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hwamee","family":"Oh","sequence":"additional","affiliation":[{"name":"Departments of Psychiatry and Human Behavior and Cognitive and Psychological Sciences, Brown University, Providence, RI, USA"},{"name":"Carney Institute for Brain Science, Brown University, Providence, RI, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"for the Alzheimer\u2019s Disease Neuroimaging Initiative","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2025,9]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13024-019-0333-5"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.3390\/biomedicines10040850"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-013-1185-7"},{"key":"e_1_3_3_5_2","article-title":"Concordance of CSF measures of Alzheimer\u2019s pathology with amyloid PET status in a preclinical cohort: a comparison of Lumipulse and established immunoassays","volume":"13","author":"Keshavan A","year":"2021","unstructured":"Keshavan A, Wellington H, Chen Z, et al. 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