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Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration

Journal article
Authors E. H. Thijssen
R. La Joie
A. Wolf
A. Strom
P. Wang
L. Iaccarino
V. Bourakova
Y. Cobigo
H. Heuer
S. Spina
L. VandeVrede
X. Y. Chai
N. K. Proctor
D. C. Airey
S. Shcherbinin
C. D. Evans
J. R. Sims
Henrik Zetterberg
Kaj Blennow
A. M. Karydas
C. E. Teunissen
J. H. Kramer
L. T. Grinberg
W. W. Seeley
H. Rosen
B. F. Boeve
B. L. Miller
G. D. Rabinovici
J. L. Dage
J. C. Rojas
A. L. Boxer
Published in Nature Medicine
Volume 26
Pages 387-397
ISSN 1078-8956
Publication year 2020
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 387-397
Language en
Keywords positron-emission-tomography, neurofilament light-chain, mild cognitive, impairment, csf biomarkers, association workgroups, national institute, fluid biomarkers, amyloid pet, dementia, neuropathology, Biochemistry & Molecular Biology, Cell Biology, Research & Experimental, Medicine
Subject categories Biochemistry and Molecular Biology


Plasma pTau181 concentrations are elevated specifically in patients diagnosed with Alzheimer's disease compared to those diagnosed with frontotemporal lobar degeneration or elderly controls, supporting its further development as a blood-based biomarker for AD. With the potential development of new disease-modifying Alzheimer's disease (AD) therapies, simple, widely available screening tests are needed to identify which individuals, who are experiencing symptoms of cognitive or behavioral decline, should be further evaluated for initiation of treatment. A blood-based test for AD would be a less invasive and less expensive screening tool than the currently approved cerebrospinal fluid or amyloid beta positron emission tomography (PET) diagnostic tests. We examined whether plasma tau phosphorylated at residue 181 (pTau181) could differentiate between clinically diagnosed or autopsy-confirmed AD and frontotemporal lobar degeneration. Plasma pTau181 concentrations were increased by 3.5-fold in AD compared to controls and differentiated AD from both clinically diagnosed (receiver operating characteristic area under the curve of 0.894) and autopsy-confirmed frontotemporal lobar degeneration (area under the curve of 0.878). Plasma pTau181 identified individuals who were amyloid beta-PET-positive regardless of clinical diagnosis and correlated with cortical tau protein deposition measured by F-18-flortaucipir PET. Plasma pTau181 may be useful to screen for tau pathology associated with AD.

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