{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:20:59Z","timestamp":1790889659609,"version":"4.1.0"},"reference-count":111,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2025,1,29]],"date-time":"2025-01-29T00:00:00Z","timestamp":1738108800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100019179","name":"\u2018La Caixa\u2019 Foundation","doi-asserted-by":"publisher","award":["100010434"],"award-info":[{"award-number":["100010434"]}],"id":[{"id":"10.13039\/501100019179","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100019179","name":"\u2018La Caixa\u2019 Foundation","doi-asserted-by":"publisher","award":["LCF\/BQ\/EU21\/11890154"],"award-info":[{"award-number":["LCF\/BQ\/EU21\/11890154"]}],"id":[{"id":"10.13039\/501100019179","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,7,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Plasma phosphorylated tau (p-tau) biomarkers open unprecedented opportunities for identifying carriers of Alzheimer\u2019s disease pathophysiology in early disease stages using minimally invasive techniques. Plasma p-tau biomarkers are believed to reflect tau phosphorylation and secretion. However, it remains unclear to what extent the magnitude of plasma p-tau abnormalities reflects neuronal network disturbance in the form of cognitive impairment.<\/jats:p>\n               <jats:p>To address this question, we included 103 cognitively unimpaired elderly and 40 cognitively impaired, amyloid-\u03b2-positive individuals from the TRIAD cohort, in addition to 336 cognitively unimpaired and 216 cognitively impaired, amyloid-\u03b2-positive older adults from the BioFINDER-2 cohort. Participants had tau PET scans, amyloid PET scans or amyloid CSF, p-tau217, p-tau181 and p-tau231 blood measures, structural T1-MRI and cognitive assessments. In this cross-sectional study, we used regression models and correlation analyses to assess the relationship between plasma biomarkers and cognitive scores. Furthermore, we applied receiver operating characteristic curves to assess cognitive impairment across plasma biomarkers. Finally, we categorized participants into amyloid (A), p-tau (T1) and tau PET (T2) positive (+) or negative (\u2212) profiles and ran non-parametric comparisons to assess differences across cognitive domains.<\/jats:p>\n               <jats:p>We found that plasma p-tau217 was more associated with cognitive performance than p-tau181 and p-tau231 and that this relationship was particularly strong for memory scores (TRIAD: \u03b2p-tau217 = \u22120.53, \u03b2p-tau181 = \u22120.35 and \u03b2p-tau231 = \u22120.24; BioFINDER-2: \u03b2p-tau217 = \u22120.52, \u03b2p-tau181 = \u22120.24 and \u03b2p-tau231 = \u22120.29). Associations in amyloid-\u03b2-positive participants resembled these results, but other cognitive scores also showed strong associations in cognitively impaired individuals. Moreover, plasma p-tau217 outperformed plasma p-tau181 and plasma p-tau231 in identifying memory impairment (area under the curve values for TRIAD: p-tau217 = 0.86, p-tau181 = 0.77 and p-tau231 = 0.75; and for BioFINDER-2: p-tau217 = 0.86, p-tau181 = 0.76 and p-tau231 = 0.81) and in identifying executive function impairment only in the BioFINDER-2 cohort (p-tau217 = 0.82, p-tau181 = 0.76 and p-tau231 = 0.76). Lastly, we showed that subtle memory deficits were present in A+T1+T2\u2212 participants for plasma p-tau217 (P = 0.007) and plasma p-tau181 (P = 0.01) in the TRIAD cohort and for all biomarkers across cognitive domains in A+T1+T2\u2212 and A+T1+T2\u2212 individuals (P &amp;lt; 0.001 in all) in the BioFINDER-2 cohort. The A+T1+T2\u2212 individuals showed cognitive deficits in both cohorts (P &amp;lt; 0.001 in all).<\/jats:p>\n               <jats:p>Together, our results suggest that plasma p-tau217 stands out as a biomarker capable of identifying memory deficits attributable to Alzheimer\u2019s disease and that memory impairment certainly occurs in amyloid-\u03b2- and plasma p-tau-positive individuals who have no significant amounts of tau in the neocortex.<\/jats:p>","DOI":"10.1093\/brain\/awaf033","type":"journal-article","created":{"date-parts":[[2025,1,29]],"date-time":"2025-01-29T22:22:12Z","timestamp":1738189332000},"page":"2384-2399","source":"Crossref","is-referenced-by-count":42,"title":["Plasma phosphorylated tau217 strongly associates with memory deficits in the Alzheimer\u2019s disease spectrum"],"prefix":"10.1093","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6810-5920","authenticated-orcid":false,"given":"Jaime","family":"Fern\u00e1ndez Arias","sequence":"first","affiliation":[{"name":"Translational Neuroimaging Laboratory, Montreal Neurological Institute , Montreal, Quebec H3A 2B4 ,","place":["Canada"]},{"name":"Department of Neurology and Neurosurgery, McGill University Research Centre for Studies in Aging , Verdun, Quebec H4H 1R3 ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wagner S","family":"Brum","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg , M\u00f6lndal 41390 ,","place":["Sweden"]},{"name":"Graduate Program in Biological Sciences: Biochemistry, Universidade Federal do Rio Grande do Sul (UFRGS) , Porto Alegre 90010-150 ,","place":["Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5210-9230","authenticated-orcid":false,"given":"Gemma","family":"Salvad\u00f3","sequence":"additional","affiliation":[{"name":"Clinical Memory Research Unit, Department of Clinical Sciences Malm\u00f6, Faculty of Medicine, Lund University , Lund 22184 ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph","family":"Therriault","sequence":"additional","affiliation":[{"name":"Translational Neuroimaging Laboratory, Montreal Neurological Institute , Montreal, Quebec H3A 2B4 ,","place":["Canada"]},{"name":"Department of Neurology and Neurosurgery, McGill University Research Centre for Studies in Aging , Verdun, Quebec H4H 1R3 ,","place":["Canada"]},{"name":"Faculty of Medicine, McGill University , Montreal, Quebec H3G 2M1 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H3A 2B4 ,","place":["Canada"]},{"name":"D\u00e9partement de Psychologie, Universit\u00e9 du Quebec \u00e1 Montr\u00e9al , Montreal, Quebec H2L 2C4 ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nesrine","family":"Rahmouni","sequence":"additional","affiliation":[{"name":"Translational Neuroimaging Laboratory, Montreal Neurological Institute , Montreal, Quebec H3A 2B4 ,","place":["Canada"]},{"name":"Department of Neurology and Neurosurgery, McGill University Research Centre for Studies in Aging , Verdun, Quebec H4H 1R3 ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur C","family":"Macedo","sequence":"additional","affiliation":[{"name":"Translational Neuroimaging Laboratory, Montreal Neurological Institute , Montreal, Quebec H3A 2B4 ,","place":["Canada"]},{"name":"Department of Neurology and Neurosurgery, McGill University Research Centre for Studies in Aging , Verdun, Quebec H4H 1R3 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