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Plasma phosphorylated tau 217 detects amyloid-β in neuronal synuclein disease
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  • Published: 10 April 2026

Plasma phosphorylated tau 217 detects amyloid-β in neuronal synuclein disease

  • Alena M. Smith1,
  • Sara A. Lorkiewicz1,
  • Burak Arslan2,
  • Laia Montoliu-Gaya2,
  • Nicholas J. Ashton2,3,4,
  • Edward N. Wilson1,5,
  • Daniel Alcolea6,7,
  • Íñigo Rodríguez-Baz6,7,8,
  • Juan Fortea6,7,8,
  • Christina B. Young1,9,10,
  • Joseph R. Winer1,
  • Marian Shahid-Besanti1,
  • Hillary Vossler1,
  • Melanie J. Plastini1,
  • Tianyu Pan11,
  • Elena Vera-Campuzano6,7,
  • Isabel Sala6,7,
  • Justin H. Mendiola1,
  • Veronica Ramirez1,
  • Geoffrey A. Kerchner12,
  • Katrin I. Andreasson1,
  • Victor W. Henderson1,
  • Thomas J. Montine13,
  • Lu Tian14,
  • Elizabeth C. Mormino1,5,15,
  • Henrik Zetterberg2,16,17,18,19,20,21,22,
  • Kathleen L. Poston1,23 na1 &
  • …
  • Carla Abdelnour1,6,7 na1 

npj Parkinson's Disease (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Biomarkers
  • Diseases
  • Neurology
  • Neuroscience

Abstract

Multiple proteinopathies commonly coexist in neurodegenerative diseases, making it essential to evaluate plasma biomarker performance in these complex diseases. While plasma biomarkers accurately detect amyloid-β pathology in Alzheimer’s disease (AD), their performance is unknown in neuronal synuclein disease (NSD). We aimed to determine the accuracy of plasma pTau217, pTau181, Aβ42/40, GFAP, and NfL to detect amyloid-β in NSD, then establish and validate cut points for the most promising marker. We included 253 participants (180 discovery; 73 validation). In the discovery cohort, NSD status was defined by CSF α-synuclein seed amplification assay and amyloid-β status by CSF Aβ42/40. Participants included individuals with clinical Lewy body disease (LBD), AD, and cognitively unimpaired. Validation cohorts consisted of clinically diagnosed LBD participants. In the discovery cohort, plasma pTau217, pTau181, Aβ42/40, and GFAP significantly differed by amyloid-β status regardless of NSD status, while NfL was highest in NSD+/Aβ+ participants. Among all biomarkers, plasma pTau217 showed the best diagnostic performance (AUC = 0.92, 95% CI = 0.81–0.98). Applying plasma pTau217 cut points to pre-screen clinically diagnosed LBD participants reduced the need for confirmatory amyloid-β PET or CSF in 41-56%. These findings support plasma pTau217 as a minimally-invasive tool for identifying pathological amyloid-β in neuronal synucleinopathies with mixed Alzheimer’s disease pathology.

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Data availability

Data availability: The datasets generated and analyzed during the current study are not publicly available due to participant privacy and confidentiality constraints. However, anonymized data from the current study are available from the corresponding author on reasonable request, contingent upon completion of Stanford University’s data use agreement approval.

Code availability

The underlying code for this study’s statistical analysis is not publicly available but may be made available to qualified researchers upon reasonable request from the corresponding author.

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Acknowledgements

ENW received support from the Knight Initiative for Brain Resilience. DA received support from the Institute of Health Carlos III (ISCIII) grants PI18/00435, PI22/00611, INT19/00016, INT23/00048, jointly funded by Fondo Europeo de Desarrollo Regional, Unión Europea, “Una manera de hacer Europa”. VWH received support from NCRAD grant P50 AG047366, and NACC grant P30 AG066515. ECM received support from NIH grant R21AG058859. HZ is a Wallenberg Scholar and a Distinguished Professor at the Swedish Research Council supported by grants from the Swedish Research Council (#2023-00356, #2022-01018 and #2019-02397), the European Union’s Horizon Europe research and innovation programme under grant agreement No 101053962, Swedish State Support for Clinical Research (#ALFGBG-71320), the Alzheimer Drug Discovery Foundation (ADDF), USA (#201809-2016862), the AD Strategic Fund and the Alzheimer's Association (#ADSF-21-831376-C, #ADSF-21-831381-C, #ADSF-21-831377-C, and #ADSF-24-1284328-C), the European Partnership on Metrology, co-financed from the European Union’s Horizon Europe Research and Innovation Programme and by the Participating States (NEuroBioStand, #22HLT07), the Bluefield Project, Cure Alzheimer’s Fund, the Olav Thon Foundation, the Erling-Persson Family Foundation, Familjen Rönströms Stiftelse, Familjen Beiglers Stiftelse, Stiftelsen för Gamla Tjänarinnor, Hjärnfonden, Sweden (#FO2022-0270), the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 860197 (MIRIADE), the European Union Joint Programme – Neurodegenerative Disease Research (JPND2021-00694), the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre, the UK Dementia Research Institute at UCL (UKDRI-1003), and an anonymous donor. KLP received support from NIH grants K23 NS075097 and R01NS115114. CA received support from the Susan and Charles Berghoff Foundation, the ARISTOS program co-funded by the European Union's Horizon Europe research and innovation programme under the Marie Sklodowska-Curie grant agreement No 101081334, and the Spanish Institute of Health Carlos III (ISCIII) Juan Rodés grant JR25/00034. These funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Author information

Author notes

  1. These authors contributed equally: Kathleen L. Poston, Carla Abdelnour.

Authors and Affiliations

  1. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA

    Alena M. Smith, Sara A. Lorkiewicz, Edward N. Wilson, Christina B. Young, Joseph R. Winer, Marian Shahid-Besanti, Hillary Vossler, Melanie J. Plastini, Justin H. Mendiola, Veronica Ramirez, Katrin I. Andreasson, Victor W. Henderson, Elizabeth C. Mormino, Kathleen L. Poston & Carla Abdelnour

  2. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden

    Burak Arslan, Laia Montoliu-Gaya, Nicholas J. Ashton & Henrik Zetterberg

  3. Banner Alzheimer’s Institute and University of Arizona, Phoenix, AZ, USA

    Nicholas J. Ashton

  4. Banner Sun Health Research Institute, Sun City, AZ, USA

    Nicholas J. Ashton

  5. Wu Tsai Neurosciences Institute, Stanford University School of Medicine, Stanford, CA, USA

    Edward N. Wilson & Elizabeth C. Mormino

  6. Sant Pau Memory Unit, IR SANT PAU, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain

    Daniel Alcolea, Íñigo Rodríguez-Baz, Juan Fortea, Elena Vera-Campuzano, Isabel Sala & Carla Abdelnour

  7. Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain

    Daniel Alcolea, Íñigo Rodríguez-Baz, Juan Fortea, Elena Vera-Campuzano, Isabel Sala & Carla Abdelnour

  8. Barcelona Down Medical Center, Fundació Catalana de Síndrome de Down, Barcelona, Spain

    Íñigo Rodríguez-Baz & Juan Fortea

  9. Department of Radiology, University of California Davis, Davis, CA, USA

    Christina B. Young

  10. Department of Neurology, University of California Davis, Davis, CA, USA

    Christina B. Young

  11. Department of Biomedical Data Science, School of Medicine. Department of Statistics, School of Humanities and Sciences, Stanford, CA, USA

    Tianyu Pan

  12. Pharma Product Development, F. Hoffmann-La Roche, Ltd., Roche, Basel, Switzerland

    Geoffrey A. Kerchner

  13. Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA

    Thomas J. Montine

  14. Department of Epidemology and Population Health, Stanford University School of Medicine, Stanford, CA, USA

    Lu Tian

  15. Molecular Imaging Program at Stanford (MIPS), Stanford University, Stanford, CA, USA

    Elizabeth C. Mormino

  16. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden

    Henrik Zetterberg

  17. Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK

    Henrik Zetterberg

  18. UK Dementia Research Institute at UCL, London, UK

    Henrik Zetterberg

  19. Hong Kong Center for Neurodegenerative Diseases, InnoHK, Hong Kong, China

    Henrik Zetterberg

  20. Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA

    Henrik Zetterberg

  21. Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA

    Henrik Zetterberg

  22. Centre for Brain Research, Indian Institute of Science, Bangalore, India

    Henrik Zetterberg

  23. Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA

    Kathleen L. Poston

Authors
  1. Alena M. Smith
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  2. Sara A. Lorkiewicz
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Contributions

C.A. and A.M.S. had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Concept and design: C.A., K.L.P. Acquisition, analysis, or interpretation of data: C.A., A.M.S., S.A.L., K.L.P., B.A., L.M.G., N.J.A., E.N.W., D.A., I.R.B., C.B.Y., J.R.W., M.S.B., H.V., M.J.P., T.P., E.V.C., I.S., J.H.M., K.I.A., V.W.H., T.J.M., L.T., E.C.M., H.Z. Drafting of the manuscript: C.A., A.M.S., S.A.L., K.L.P. Critical review of the manuscript for important intellectual content: C.A., K.L.P., A.M.S., S.A.L., B.A., L.M.G., N.J.A., E.N.W., D.A., I.R.B., J.F., C.B.Y., J.R.W., M.S.B., H.V., M.J.P., T.P., E.V.C., I.S., J.H.M., V.R., G.A.K., K.I.A., V.W.H., T.J.M., LT, E.C.M., H.Z.Statistical analysis: C.A., A.M.S., S.A.L.Obtained funding: C.A., K.L.P. Administrative, technical, or material support: C.A., K.L.P., A.M.S., S.A.L., B.A., L.M.G., N.J.A., E.N.W., D.A., I.R.B., J.F., H.V., T.P., J.H.M., V.R., G.A.K., V.W.H., T.J.M., L.T., E.C.M., H.Z. Statistical analysis: C.A., A.M.S., S.A.L. Obtained funding: E.N.W., D.A., V.W.H., H.Z., K.L.P., C.A. Administrative, technical, or material support: C.A., K.L.P., A.M.S., S.A.L., B.A., L.M.G., N.J.A., E.N.W., D.A., I.R.B., J.F., H.V., T.P., J.H.M., V.R., G.A.K., V.W.H., T.J.M., L.T., E.C.M., H.Z. Supervision: C.A., K.L.P.

Corresponding author

Correspondence to Carla Abdelnour.

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Competing interests

These authors declare competing interests: LMG has received speaker fees from Quanterix and Esteve and served as a consultant for Quanterix. MJP is currently a full-time employee at Amprion Inc. DA has participated in advisory boards for Fujirebio-Europe, Roche Diagnostics, Grifols S.A. and Lilly, and received speaker honoraria from Fujirebio-Europe, Roche Diagnostics, Nutricia, Krka Farmacéutica S.L., Zambon S.A.U., Neuraxpharm, Alter Medica, Lilly and Esteve Pharmaceuticals S.A. DA holds a patent for markers of synaptopathy in neurodegenerative disease (licensed to ADx NeuroSciences N.V., WO2019175379 Markers of synaptopathy in neurodegenerative diseases). JF has served on advisory boards, adjudication committees, or speaker honoraria from AC Immune, Adamed, Alzheon, Biogen, Eisai, Esteve, Fujirebio, Ionis, Laboratorios Carnot, Life Molecular Imaging, Lilly, Lundbeck, Novo Nordisk, Perha, Roche, Zambon, Spanish Neurological Society, T21 Research Society, Lumind Foundation, Jérôme-Lejeune Foundation, Alzheimer’s Association, National Institutes of Health USA, and Instituto de Salud Carlos III. JF also holds a patent for markers of synaptopathy in neurodegenerative disease (licensed to ADx NeuroSciences N.V., WO2019175379 Markers of synaptopathy in neurodegenerative diseases). HZ has served at scientific advisory boards and/or as a consultant for Abbvie, Acumen, Alector, Alzinova, ALZpath, Amylyx, Annexon, Apellis, Artery Therapeutics, AZTherapies, Cognito Therapeutics, CogRx, Denali, Eisai, Enigma, LabCorp, Merck Sharp & Dohme, Merry Life, Nervgen, Novo Nordisk, Optoceutics, Passage Bio, Pinteon Therapeutics, Prothena, Quanterix, Red Abbey Labs, reMYND, Roche, Samumed, ScandiBio Therapeutics AB, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures sponsored by Alzecure, BioArctic, Biogen, Cellectricon, Fujirebio, LabCorp, Lilly, Novo Nordisk, Oy Medix Biochemica AB, Roche, and WebMD, is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program, and is a shareholder of MicThera (outside submitted work). KLP has been on the Scientific Advisory Board for Amprion and has been a consultant for Novartis, Lilly, BioArctic, Biohaven, Curasen and Neuron23. CA has received honoraria as a speaker from Hoffman-La Roche LTD, Nutricia, Schwabe Farma Ibérica SAU and Zambon; and is a member of the Board of Directors of the Lewy Body Dementia Association, the Scientific Committee of Lewy Body España, and the Alzheimer’s Association International Society to Advance Alzheimer’s Research and Treatment (ISTAART) Advisory Council. All other authors (AMS, SAL, BA, NJA, ENW, IRB, CBY, JRW, MSB, HV, TP, EVC, IS, JHM, VR, GAK, KIA, VWH, TJM, LT, and ECM) declare no financial or non-financial competing interests. No authors have pending patent applications related to the work described in this manuscript.

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Smith, A.M., Lorkiewicz, S.A., Arslan, B. et al. Plasma phosphorylated tau 217 detects amyloid-β in neuronal synuclein disease. npj Parkinsons Dis. (2026). https://doi.org/10.1038/s41531-026-01341-8

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  • Received: 17 January 2026

  • Accepted: 25 March 2026

  • Published: 10 April 2026

  • DOI: https://doi.org/10.1038/s41531-026-01341-8

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