Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease

Fernando Gonzalez-Ortiz (), Bjørn-Eivind Kirsebom, José Contador, Jordan E. Tanley, Per Selnes, Berglind Gísladóttir, Lene Pålhaugen, Mathilde Suhr Hemminghyth, Jonas Jarholm, Ragnhild Skogseth, Geir Bråthen, Gøril Grøndtvedt, Atle Bjørnerud, Sandra Tecelao, Knut Waterloo, Dag Aarsland, Aida Fernández-Lebrero, Greta García-Escobar, Irene Navalpotro-Gómez, Michael Turton, Agnes Hesthamar, Przemyslaw R. Kac, Johanna Nilsson, Jose Luchsinger, Kathleen M. Hayden, Peter Harrison, Albert Puig-Pijoan, Henrik Zetterberg, Timothy M. Hughes, Marc Suárez-Calvet, Thomas K. Karikari, Tormod Fladby and Kaj Blennow
Additional contact information
Fernando Gonzalez-Ortiz: the Sahlgrenska Academy at the University of Gothenburg
Bjørn-Eivind Kirsebom: University Hospital of North Norway
José Contador: Pasqual Maragall Foundation
Jordan E. Tanley: Wake Forest University School of Medicine
Per Selnes: Akershus University Hospital
Berglind Gísladóttir: Akershus University Hospital
Lene Pålhaugen: Akershus University Hospital
Mathilde Suhr Hemminghyth: Haugesund Hospital
Jonas Jarholm: Akershus University Hospital
Ragnhild Skogseth: Haraldsplass Deaconess Hospital
Geir Bråthen: University Hospital of Trondheim
Gøril Grøndtvedt: University Hospital of Trondheim
Atle Bjørnerud: University of Oslo
Sandra Tecelao: Akershus University Hospital
Knut Waterloo: University Hospital of North Norway
Dag Aarsland: Psychology and Neuroscience King’s College London
Aida Fernández-Lebrero: Pasqual Maragall Foundation
Greta García-Escobar: Hospital del Mar Research Institute
Irene Navalpotro-Gómez: Pasqual Maragall Foundation
Michael Turton: Bioventix Plc
Agnes Hesthamar: the Sahlgrenska Academy at the University of Gothenburg
Przemyslaw R. Kac: the Sahlgrenska Academy at the University of Gothenburg
Johanna Nilsson: the Sahlgrenska Academy at the University of Gothenburg
Jose Luchsinger: Wake Forest University School of Medicine
Kathleen M. Hayden: Wake Forest University School of Medicine
Peter Harrison: Bioventix Plc
Albert Puig-Pijoan: Pasqual Maragall Foundation
Henrik Zetterberg: the Sahlgrenska Academy at the University of Gothenburg
Timothy M. Hughes: Wake Forest University School of Medicine
Marc Suárez-Calvet: Pasqual Maragall Foundation
Thomas K. Karikari: the Sahlgrenska Academy at the University of Gothenburg
Tormod Fladby: University of Oslo
Kaj Blennow: the Sahlgrenska Academy at the University of Gothenburg

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Staging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer’s disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking. In this multicenter study (n = 1076), we show that brain-derived tau (BD-tau) in blood increases according to concomitant Aβ (“A”) and neurodegeneration (“N”) abnormalities (determined using cerebrospinal fluid biomarkers); We used blood-based A/N biomarkers to profile the participants in this study; individuals with blood-based p-tau+/BD-tau+ profiles had the fastest cognitive decline and atrophy rates, irrespective of the baseline cognitive status. Furthermore, BD-tau showed no or much weaker correlations with age, renal function, other comorbidities/risk factors and self-identified race/ethnicity, compared with other blood biomarkers. Here we show that blood-based BD-tau is a biomarker for identifying Aβ-positive individuals at risk of short-term cognitive decline and atrophy, with implications for clinical trials and implementation of anti-Aβ therapies.

Date: 2024
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DOI: 10.1038/s41467-024-47286-5

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