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, Kaj Blennow
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...
April 4, 2024: Nature Communications