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In a cohort with post\u2010mortem neuropathological data (\n                    <jats:italic>N<\/jats:italic>\n                    \u00a0=\u00a088), both plaque and tangle density contributed independently to higher P\u2010tau217, but P\u2010tau217 was not elevated in patients with non\u2010Alzheimer\u2019s disease tauopathies (\n                    <jats:italic>N<\/jats:italic>\n                    \u00a0=\u00a09). Several findings were replicated in a cohort with PET imaging (\u201cBioFINDER\u20102\u201d,\n                    <jats:italic>N<\/jats:italic>\n                    \u00a0=\u00a0426), where \u03b2\u2010amyloid and tau PET were independently associated with P\u2010tau217. P\u2010tau217 concentrations correlated with \u03b2\u2010amyloid PET (but not tau PET) in early disease stages and with both \u03b2\u2010amyloid and (more strongly) tau PET in late disease stages. Finally, P\u2010tau217 mediated the association between \u03b2\u2010amyloid and tau in both cohorts, especially for tau outside of the medial temporal lobe. These findings support the hypothesis that plasma P\u2010tau217 concentration is increased by both \u03b2\u2010amyloid plaques and tau tangles and is congruent with the hypothesis that P\u2010tau is involved in \u03b2\u2010amyloid\u2010dependent formation of neocortical tau tangles.\n                  <\/jats:p>","DOI":"10.15252\/emmm.202114022","type":"journal-article","created":{"date-parts":[[2021,5,5]],"date-time":"2021-05-05T07:27:23Z","timestamp":1620199643000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":263,"title":["Soluble P\u2010tau217 reflects amyloid and tau pathology and mediates the association of amyloid with tau"],"prefix":"10.1038","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8885-7724","authenticated-orcid":false,"given":"Niklas","family":"Mattsson\u2010Carlgren","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shorena","family":"Janelidze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Randall J","family":"Bateman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruben","family":"Smith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Stomrud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geidy E","family":"Serrano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric M","family":"Reiman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9267-1930","authenticated-orcid":false,"given":"Sebastian","family":"Palmqvist","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey L","family":"Dage","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas G","family":"Beach","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8467-7286","authenticated-orcid":false,"given":"Oskar","family":"Hansson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,5,5]]},"reference":[{"key":"BFEMMM202114022_CR1","doi-asserted-by":"crossref","DOI":"10.1084\/jem.20200861","volume":"217","author":"NR Barth\u00e9lemy","year":"2020","unstructured":"Barth\u00e9lemy NR, Horie K, Sato C, Bateman RJ (2020a) Blood plasma phosphorylated\u2010tau isoforms track CNS change in Alzheimer\u2019s disease. 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In the past 2\u00a0years, he has received consultancy\/speaker fees from AC Immune, Alzpath, Biogen, Cerveau, and Roche. NMC, ES, SP, SJ, and RS have no disclosures. TGB has had research support from the National Institute on Aging, Michael J Fox Foundation for Parkinson\u2019s Research, and the State of Arizona and, in the past 2\u00a0years, has received consultancy and\/or speaker fees from Prothena Biosciences and Vivid Genomics. JLD is an employee of Eli Lilly and Company. Remaining co\u2010authors report no disclosures.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}}],"article-number":"EMMM202114022"}}