Details

Autor(en) / Beteiligte

• 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
• Luchsinger, Jose
• Hayden, Kathleen M
• Harrison, Peter
• Puig-Pijoan, Albert
• Zetterberg, Henrik
• Hughes, Timothy M
• Suárez-Calvet, Marc
• Karikari, Thomas K
• Fladby, Tormod
• Blennow, Kaj

Titel

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

Ist Teil von

• Nature communications, 2024-04, Vol.15 (1), p.2908-2908, Article 2908

Ort / Verlag

England: Nature Publishing Group

Erscheinungsjahr

2024

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.