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Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism

The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer’s Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking. This may require a better in depth understanding of the cascade. Particularly,...

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Autores principales: Stancu, Ilie-Cosmin, Vasconcelos, Bruno, Terwel, Dick, Dewachter, Ilse
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255655/
https://www.ncbi.nlm.nih.gov/pubmed/25407337
http://dx.doi.org/10.1186/1750-1326-9-51
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author Stancu, Ilie-Cosmin
Vasconcelos, Bruno
Terwel, Dick
Dewachter, Ilse
author_facet Stancu, Ilie-Cosmin
Vasconcelos, Bruno
Terwel, Dick
Dewachter, Ilse
author_sort Stancu, Ilie-Cosmin
collection PubMed
description The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer’s Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking. This may require a better in depth understanding of the cascade. Particularly, the exact toxic forms of Aβ and Tau, the molecular link between them and their respective contributions to the disease process need to be identified in detail. Although the lack of final proof has raised substantial criticism on the hypothesis per se, accumulating experimental evidence in in vitro models, in vivo models and from biomarkers analysis in patients supports the amyloid cascade and particularly Aβ-induced Tau-pathology, which is the focus of this review. We here discuss available models that recapitulate Aβ-induced Tau-pathology and review some potential underlying mechanisms. The availability and diversity of these models that mimic the amyloid cascade partially or more complete, provide tools to study remaining questions, which are crucial for development of therapeutic strategies for Alzheimer’s Disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1750-1326-9-51) contains supplementary material, which is available to authorized users.
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spelling pubmed-42556552014-12-05 Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism Stancu, Ilie-Cosmin Vasconcelos, Bruno Terwel, Dick Dewachter, Ilse Mol Neurodegener Review The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer’s Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking. This may require a better in depth understanding of the cascade. Particularly, the exact toxic forms of Aβ and Tau, the molecular link between them and their respective contributions to the disease process need to be identified in detail. Although the lack of final proof has raised substantial criticism on the hypothesis per se, accumulating experimental evidence in in vitro models, in vivo models and from biomarkers analysis in patients supports the amyloid cascade and particularly Aβ-induced Tau-pathology, which is the focus of this review. We here discuss available models that recapitulate Aβ-induced Tau-pathology and review some potential underlying mechanisms. The availability and diversity of these models that mimic the amyloid cascade partially or more complete, provide tools to study remaining questions, which are crucial for development of therapeutic strategies for Alzheimer’s Disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1750-1326-9-51) contains supplementary material, which is available to authorized users. BioMed Central 2014-11-18 /pmc/articles/PMC4255655/ /pubmed/25407337 http://dx.doi.org/10.1186/1750-1326-9-51 Text en © Stancu et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Stancu, Ilie-Cosmin
Vasconcelos, Bruno
Terwel, Dick
Dewachter, Ilse
Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title_full Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title_fullStr Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title_full_unstemmed Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title_short Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
title_sort models of β-amyloid induced tau-pathology: the long and “folded” road to understand the mechanism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255655/
https://www.ncbi.nlm.nih.gov/pubmed/25407337
http://dx.doi.org/10.1186/1750-1326-9-51
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