학술논문
Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer's disease.
Document Type
Author
Gonzalez-Ortiz, Fernando; Kirsebom, Bjørn-Eivind; Contador, José; Tanley, Jordan E; Selnes, Per; Gísladóttir, Berglind; Pålhaugen, Lene; Suhr Hemminghyth, Mathilde; Jarholm, Jonas; Skogseth, Ragnhild; Bråthen, Geir; Grøndtvedt, Gøril; Bjørnerud, Atle; Tecelao, Sandra; Waterloo, Knut; Aarsland, Dag; Fernández-Lebrero, Aida; García-Escobar, Greta; Navalpotro-Gómez, Irene; Turton, Michael; Hesthamar, Agnes; Kac, Przemyslaw R.; Nilsson, Johanna, 1993; Luchsinger, Jose; Hayden, Kathleen M; Harrison, Peter; Puig-Pijoan, Albert; Zetterberg, Henrik, 1973; Hughes, Timothy M; Suárez-Calvet, Marc; Karikari, Thomas; Fladby, Tormod; Blennow, Kaj, 1958
Source
Nature communications. 15(1)
Subject
Language
English
ISSN
2041-1723
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.