Author
Listed:
- Fernando Gonzalez-Ortiz
(the Sahlgrenska Academy at the University of Gothenburg
Sahlgrenska University Hospital)
- Bjørn-Eivind Kirsebom
(University Hospital of North Norway
The Arctic University of Norway
University of Oslo)
- José Contador
(Pasqual Maragall Foundation
Hospital del Mar Research Institute
Hospital del Mar)
- 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
Haugesund Hospital
University of Bergen)
- Jonas Jarholm
(Akershus University Hospital)
- Ragnhild Skogseth
(Haraldsplass Deaconess Hospital
University of Bergen)
- Geir Bråthen
(University Hospital of Trondheim
Norwegian University of Science and Technology)
- Gøril Grøndtvedt
(University Hospital of Trondheim
Norwegian University of Science and Technology)
- Atle Bjørnerud
(University of Oslo
Oslo University hospital
University of Oslo)
- Sandra Tecelao
(Akershus University Hospital)
- Knut Waterloo
(University Hospital of North Norway
The Arctic University of Norway)
- Dag Aarsland
(Psychology and Neuroscience King’s College London
Centre for Age-Related Diseases, University Hospital Stavanger)
- Aida Fernández-Lebrero
(Pasqual Maragall Foundation
Hospital del Mar Research Institute
Hospital del Mar
Universitat Pompeu Fabra)
- Greta García-Escobar
(Hospital del Mar Research Institute
ERA-Net on Cardiovascular Diseases (ERA-CVD) consortium)
- Irene Navalpotro-Gómez
(Pasqual Maragall Foundation
Hospital del Mar Research Institute
Hospital del Mar
ERA-Net on Cardiovascular Diseases (ERA-CVD) consortium)
- 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
Hospital del Mar Research Institute
ERA-Net on Cardiovascular Diseases (ERA-CVD) consortium
Universitat Autònoma de Barcelona)
- Henrik Zetterberg
(the Sahlgrenska Academy at the University of Gothenburg
Sahlgrenska University Hospital
Queen Square
UK Dementia Research Institute at UCL)
- Timothy M. Hughes
(Wake Forest University School of Medicine)
- Marc Suárez-Calvet
(Pasqual Maragall Foundation
Hospital del Mar Research Institute
Hospital del Mar
Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERFES))
- Thomas K. Karikari
(the Sahlgrenska Academy at the University of Gothenburg
University of Pittsburgh)
- Tormod Fladby
(University of Oslo
Akershus University Hospital)
- Kaj Blennow
(the Sahlgrenska Academy at the University of Gothenburg
Sahlgrenska University Hospital)
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.
Suggested Citation
Fernando Gonzalez-Ortiz & Bjørn-Eivind Kirsebom & José Contador & Jordan E. Tanley & Per Selnes & Berglind Gísladóttir & Lene Pålhaugen & Mathilde Suhr Hemminghyth & Jonas Jarholm & Ragnhild Skogseth , 2024.
"Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease,"
Nature Communications, Nature, vol. 15(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-47286-5
DOI: 10.1038/s41467-024-47286-5
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