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024 7 _ |a 10.1007/s00259-021-05258-7
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024 7 _ |a 1432-105X
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024 7 _ |a 1619-7070
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024 7 _ |a 1619-7089
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037 _ _ |a DZNE-2021-00635
082 _ _ |a 610
100 1 _ |a Leuzy, A.
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245 _ _ |a 2020 update on the clinical validity of cerebrospinal fluid amyloid, tau, and phospho-tau as biomarkers for Alzheimer’s disease in the context of a structured 5-phase development framework
260 _ _ |a Heidelberg [u.a.]
|c 2021
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520 _ _ |a Purpose: In the last decade, the research community has focused on defining reliable biomarkers for the early detection of Alzheimer's disease (AD) pathology. In 2017, the Geneva AD Biomarker Roadmap Initiative adapted a framework for the systematic validation of oncological biomarkers to cerebrospinal fluid (CSF) AD biomarkers-encompassing the 42 amino-acid isoform of amyloid-β (Aβ42), phosphorylated-tau (P-tau), and Total-tau (T-tau)-with the aim to accelerate their development and clinical implementation. The aim of this work is to update the current validation status of CSF AD biomarkers based on the Biomarker Roadmap methodology.Methods: A panel of experts in AD biomarkers convened in November 2019 at a 2-day workshop in Geneva. The level of maturity (fully achieved, partly achieved, preliminary evidence, not achieved, unsuccessful) of CSF AD biomarkers was assessed based on the Biomarker Roadmap methodology before the meeting and presented and discussed during the workshop.Results: By comparison to the previous 2017 Geneva Roadmap meeting, the primary advances in CSF AD biomarkers have been in the area of a unified protocol for CSF sampling, handling and storage, the introduction of certified reference methods and materials for Aβ42, and the introduction of fully automated assays. Additional advances have occurred in the form of defining thresholds for biomarker positivity and assessing the impact of covariates on their discriminatory ability.Conclusions: Though much has been achieved for phases one through three, much work remains in phases four (real world performance) and five (assessment of impact/cost). To a large degree, this will depend on the availability of disease-modifying treatments for AD, given these will make accurate and generally available diagnostic tools key to initiate therapy.
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650 _ 2 |a Alzheimer Disease: diagnosis
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides
|2 MeSH
650 _ 2 |a Biomarkers
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Peptide Fragments
|2 MeSH
650 _ 2 |a tau Proteins
|2 MeSH
700 1 _ |a Ashton, N. J.
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700 1 _ |a Mattsson-Carlgren, N.
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700 1 _ |a Dodich, A.
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700 1 _ |a Boccardi, M.
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700 1 _ |a Corre, J.
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700 1 _ |a Drzezga, Alexander
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700 1 _ |a Nordberg, A.
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700 1 _ |a Ossenkoppele, R.
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700 1 _ |a Zetterberg, H.
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700 1 _ |a Blennow, K.
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700 1 _ |a Frisoni, G. B.
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700 1 _ |a Garibotto, V.
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700 1 _ |a Hansson, O.
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773 _ _ |a 10.1007/s00259-021-05258-7
|g Vol. 48, no. 7, p. 2121 - 2139
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|t European journal of nuclear medicine and molecular imaging
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