Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease
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...
Ausführliche Beschreibung
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Englisch |
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2024 |
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In: Nature Communications - Nature Portfolio, 2016, 15(2024), 1, Seite 13 |
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Übergeordnetes Werk: |
volume:15 ; year:2024 ; number:1 ; pages:13 |
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DOI / URN: |
10.1038/s41467-024-47286-5 |
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DOAJ095856501 |
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10.1038/s41467-024-47286-5 doi (DE-627)DOAJ095856501 (DE-599)DOAJb027901016fa4e8ba7386d92b8d8e45e DE-627 ger DE-627 rakwb eng Fernando Gonzalez-Ortiz verfasserin aut Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. Science Q Bjørn-Eivind Kirsebom verfasserin aut José Contador verfasserin aut Jordan E. Tanley verfasserin aut Per Selnes verfasserin aut Berglind Gísladóttir verfasserin aut Lene Pålhaugen verfasserin aut Mathilde Suhr Hemminghyth verfasserin aut Jonas Jarholm verfasserin aut Ragnhild Skogseth verfasserin aut Geir Bråthen verfasserin aut Gøril Grøndtvedt verfasserin aut Atle Bjørnerud verfasserin aut Sandra Tecelao verfasserin aut Knut Waterloo verfasserin aut Dag Aarsland verfasserin aut Aida Fernández-Lebrero verfasserin aut Greta García-Escobar verfasserin aut Irene Navalpotro-Gómez verfasserin aut Michael Turton verfasserin aut Agnes Hesthamar verfasserin aut Przemyslaw R. Kac verfasserin aut Johanna Nilsson verfasserin aut Jose Luchsinger verfasserin aut Kathleen M. Hayden verfasserin aut Peter Harrison verfasserin aut Albert Puig-Pijoan verfasserin aut Henrik Zetterberg verfasserin aut Timothy M. Hughes verfasserin aut Marc Suárez-Calvet verfasserin aut Thomas K. Karikari verfasserin aut Tormod Fladby verfasserin aut Kaj Blennow verfasserin aut In Nature Communications Nature Portfolio, 2016 15(2024), 1, Seite 13 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:15 year:2024 number:1 pages:13 https://doi.org/10.1038/s41467-024-47286-5 kostenfrei https://doaj.org/article/b027901016fa4e8ba7386d92b8d8e45e kostenfrei https://doi.org/10.1038/s41467-024-47286-5 kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2024 1 13 |
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Fernando Gonzalez-Ortiz @@aut@@ Bjørn-Eivind Kirsebom @@aut@@ José Contador @@aut@@ Jordan E. Tanley @@aut@@ Per Selnes @@aut@@ Berglind Gísladóttir @@aut@@ Lene Pålhaugen @@aut@@ Mathilde Suhr Hemminghyth @@aut@@ Jonas Jarholm @@aut@@ Ragnhild Skogseth @@aut@@ Geir Bråthen @@aut@@ Gøril Grøndtvedt @@aut@@ Atle Bjørnerud @@aut@@ Sandra Tecelao @@aut@@ Knut Waterloo @@aut@@ Dag Aarsland @@aut@@ Aida Fernández-Lebrero @@aut@@ Greta García-Escobar @@aut@@ Irene Navalpotro-Gómez @@aut@@ Michael Turton @@aut@@ Agnes Hesthamar @@aut@@ Przemyslaw R. Kac @@aut@@ Johanna Nilsson @@aut@@ Jose Luchsinger @@aut@@ Kathleen M. Hayden @@aut@@ Peter Harrison @@aut@@ Albert Puig-Pijoan @@aut@@ Henrik Zetterberg @@aut@@ Timothy M. Hughes @@aut@@ Marc Suárez-Calvet @@aut@@ Thomas K. Karikari @@aut@@ Tormod Fladby @@aut@@ Kaj Blennow @@aut@@ |
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Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease |
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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. |
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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. |
abstract_unstemmed |
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. |
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Plasma brain-derived tau is an amyloid-associated neurodegeneration biomarker in Alzheimer’s disease |
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score |
7.402915 |