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A beta deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer's disease

Journal article
Authors N. Mattsson-Carlgren
E. Andersson
S. Janelidze
R. Ossenkoppele
P. Insel
O. Strandberg
Henrik Zetterberg
H. J. Rosen
G. Rabinovici
X. Y. Chai
Kaj Blennow
J. L. Dage
E. Stomrud
R. Smith
S. Palmqvist
O. Hansson
Published in Science Advances
Volume 6
Issue 16
Pages 13
ISSN 2375-2548
Publication year 2020
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Pages 13
Language en
Links dx.doi.org/10.1126/sciadv.aaz2387
Keywords positron-emission-tomography, csf t-tau, neurofibrillary pathology, cognitive decline, p-tau, markers, neurodegeneration, f-18-av-1451, aggregation, biomarkers, Science & Technology - Other Topics
Subject categories Neurosciences

Abstract

The links between beta-amyloid ( A beta ) and tau in Alzheimer's disease are unclear. Cognitively unimpaired persons with signs of A beta pathology had increased cerebrospinal fluid (CSF) phosphorylated tau (P-tau181 and P-tau217) and total-tau (T-tau), which increased over time, despite no detection of insoluble tau aggregates [normal Tau positron emission tomography (PET)]. CSF P-tau and T-tau started to increase before the threshold for Amyloid PET positivity, while Tau PET started to increase after Amyloid PET positivity. Effects of Amyloid PET on Tau PET were mediated by CSF P-tau, and high CSF P-tau predicted increased Tau PET rates. Individuals with MAPT mutations and signs of tau deposition (but without A beta pathology) had normal CSF P-tau levels. In 5xFAD mice, CSF tau increased when A beta aggregation started. These results show that A beta pathology may induce changes in soluble tau release and phosphorylation, which is followed by tau aggregation several years later in humans.

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Denna text är utskriven från följande webbsida:
http://www.gu.se/english/research/publication/?publicationId=293709
Utskriftsdatum: 2020-08-10