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Here we assess which markers can best identify AD from controls and other non\u2010AD dementias in a large international multi\u2010center study.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>Plasma samples (<jats:italic>n<\/jats:italic>\u00a0=\u00a01298) were collected from six international centers. A\u03b240, A\u03b242, GFAP, NfL, and p\u2010tau181 were measured using single molecule array. In each group, AD diagnosis\/co\u2010pathology was defined according to cerebrospinal fluid biomarkers or amyloid positron emission tomography. Validations were performed in three separate cohorts via single and dual cut\u2010off models.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>p\u2010tau181 showed the best area under the curve value to separate AD from frontotemporal dementia, controls, and A\u03b2\u2013 dementia with Lewy bodies. However, this discriminative power could not be reproduced by applying pre\u2010defined cut\u2010offs.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>p\u2010tau181 was the best single plasma marker for detecting AD at any stage. Specific cut\u2010offs are needed to maximize diagnostic performances.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Phosphorylated tau (p\u2010tau)181 provided a clear differentiation between controls and Alzheimer's disease (AD) participants, with evidence of increased levels in the preclinical stage of AD.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Plasma biomarkers demonstrated that when amyloid co\u2010pathology is removed from dementia with Lewy bodies (DLB), only glial fibrillary acidic protein and neurofilament light chain remain to predict DLB.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Given the low prevalence of amyloid co\u2010pathology in frontotemporal dementia (FTD), p\u2010tau181 and its ratio with amyloid beta 42 are strong biomarkers to differentiate FTD from AD.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.14573","type":"journal-article","created":{"date-parts":[[2025,6,23]],"date-time":"2025-06-23T23:40:22Z","timestamp":1750722022000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Diagnostic performance of plasma A\u03b242\/40 ratio, p\u2010tau181, GFAP, and NfL along the continuum of Alzheimer's disease and non\u2010AD dementias: An international multi\u2010center study"],"prefix":"10.1002","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2863-0293","authenticated-orcid":false,"given":"James D.","family":"Doecke","sequence":"first","affiliation":[{"name":"Australian E\u2010Health Research Centre CSIRO  Herston Queensland Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovanni","family":"Bellomo","sequence":"additional","affiliation":[{"name":"Section of Neurology Laboratory of 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