Capacity for Seeding and Spreading of Argyrophilic Grain Disease in a Wild-Type Murine Model; Comparisons With Primary Age-Related Tauopathy
- 1Department of Pathology and Experimental Therapeutics, University of Barcelona, Barcelona, Spain
- 2Bellvitge University Hospital, IDIBELL (Bellvitge Biomedical Research Centre), Barcelona, Spain
- 3CIBERNED (Network Centre of Biomedical Research of Neurodegenerative Diseases), Institute of Health Carlos III, Ministry of Economy and Competitiveness, Madrid, Spain
- 4Institute of Neurosciences, University of Barcelona, Barcelona, Spain
- 5Molecular and Cellular Neurobiotechnology, Institute of Bioengineering of Catalonia (IBEC), Institute for Science and Technology, Parc Científic de Barcelona, Barcelona, Spain
- 6Department of Cell Biology, Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain
A Corrigendum on
Capacity for Seeding and Spreading of Argyrophilic Grain Disease in a Wild-Type Murine Model; Comparisons With Primary Age-Related Tauopathy
by Ferrer, I., Andrés-Benito, P., Sala-Jarque, J., Gil, V., and del Rio, J. A. (2020). Front. Mol. Neurosci. 13:101. doi: 10.3389/fnmol.2020.00101
In the original article, there was a mistake in Figure 4 as published. Panels A, B, C, D, E, F of the published Figure 4 were incorrectly labeled. The corrected Figure 4 appears below.
Figure 4. Hyper-phosphorylated tau-containing cells and threads following unilateral intra-hippocampal injection of sarkosyl-insoluble fractions from PART into WT mice at the age of 7 months and killed at the age of 10 months (3 months survival) (A,C); 3 months and killed at the age of 10 months (C,D–F); and at the age of 12 months and killed at the age of 19 months (7 months survival) (G–J). Tau deposits in neurons, independently of the survival time, show granular deposits in the cytoplasm, and occasional denser inclusions with no similarities with tangles (A,B). Threads and coiled bodies are abundant in the fimbria and corpus callosum (C–F). Individual neurons, threads and oligodendrocytes in inoculated mice are stained with anti-4Rtau (G,H) and anti-3Rtau (I,J) antibodies. Paraffin sections slightly counterstained with hematoxylin. CA1, region of the hippocampus; fimbr, fimbria; ipsi contr CC, ipsi- and contralateral corpus callosum; (A–F), bar = 50 μm; (G–J), bar = 50 μm.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: argyrophilic grain disease, primary age-related tauopathy, tauopathies, tau, seeding, progression, coiled bodies
Citation: Ferrer I, Andrés-Benito P, Sala-Jarque J, Gil V and del Rio JA (2022) Corrigendum: Capacity for Seeding and Spreading of Argyrophilic Grain Disease in a Wild-Type Murine Model; Comparisons With Primary Age-Related Tauopathy. Front. Mol. Neurosci. 15:870475. doi: 10.3389/fnmol.2022.870475
Received: 06 February 2022; Accepted: 22 February 2022;
Published: 18 March 2022.
Edited and reviewed by: Gregg E. Homanics, University of Pittsburgh, United States
Copyright © 2022 Ferrer, Andrés-Benito, Sala-Jarque, Gil and del Rio. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Isidro Ferrer, ODA4MmlmYSYjeDAwMDQwO2dtYWlsLmNvbQ==