Invited Review
Prion-like transmission and spreading of tau pathology Florence
Clavaguera1, Jürgen Hench1, Michel Goedert2 and Markus Tolnay1,* DOI:
10.1111/nan.12197
This article is protected by copyright. All rights reserved.
Additional Information(Hide All) Author InformationPublication History
Author Information 1 Institute of Pathology, University Hospital Basel,
Schönbeinstrasse 40, CH-4031 Basel, Switzerland 2 MRC Laboratory of Molecular
Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK * Please send
correspondence to Markus Tolnay at the above address. Email:
markus.tolnay@usb.ch
This article has been accepted for publication and undergone full peer
review but has not been through the copyediting, typesetting, pagination and
proofreading process, which may lead to differences between this version and the
Version of Record. Please cite this article as doi: 10.1111/nan.12197
Publication History Accepted manuscript online: 17 NOV 2014 01:23AM EST
Manuscript Accepted: 13 NOV 2014
Abstract
Filaments made of hyperphosphorylated tau protein are encountered in a
number of neurodegenerative diseases referred to as “tauopathies”. In the most
prevalent tauopathy, Alzheimer's disease, tau pathology progresses in a
stereotypical manner with the first lesions appearing in the locus coeruleus and
the entorhinal cortex from where they appear to spread to the hippocampus and
neocortex. Propagation of tau pathology is also characteristic of argyrophilic
grain disease, where the tau lesions appear to spread throughout distinct
regions of the limbic system. These findings strongly implicate neuron-to-neuron
propagation of tau aggregates. Isoform composition and morphology of tau
filaments can differ between tauopathies suggesting the existence of
conformationally diverse tau strains. ***Altogether, this points to prion-like
mechanisms in the pathogenesis of tauopathies.
http://onlinelibrary.wiley.com/doi/10.1111/nan.12197/abstract?campaign=wolacceptedarticle
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
Wednesday, June 19, 2013
Spreading of tau pathology in Alzheimer's disease by cell-to-cell
transmission
Saturday, May 25, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse
brain
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic
Creutzfeldt-Jakob Disease
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type
prion disease, what it ???
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
TSS
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