Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease

The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid β (Aβ) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. However, all attempts to develop Aβ-targeting drug...

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Autores principales: Kametani, Fuyuki, Hasegawa, Masato
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Neuroscience
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5797629/
https://www.ncbi.nlm.nih.gov/pubmed/29440986
http://dx.doi.org/10.3389/fnins.2018.00025
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author Kametani, Fuyuki
Hasegawa, Masato
author_facet Kametani, Fuyuki
Hasegawa, Masato
author_sort Kametani, Fuyuki
collection PubMed
description The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid β (Aβ) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. However, all attempts to develop Aβ-targeting drugs to treat AD have ended in failure. Here, we review recent findings indicating that the main factor underlying the development and progression of AD is tau, not Aβ, and we describe the deficiencies of the amyloid hypothesis that have supported the emergence of this idea.
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spelling pubmed-57976292018-02-13 Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease Kametani, Fuyuki Hasegawa, Masato Front Neurosci Neuroscience The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid β (Aβ) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. However, all attempts to develop Aβ-targeting drugs to treat AD have ended in failure. Here, we review recent findings indicating that the main factor underlying the development and progression of AD is tau, not Aβ, and we describe the deficiencies of the amyloid hypothesis that have supported the emergence of this idea. Frontiers Media S.A. 2018-01-30 /pmc/articles/PMC5797629/ /pubmed/29440986 http://dx.doi.org/10.3389/fnins.2018.00025 Text en Copyright © 2018 Kametani and Hasegawa. http://creativecommons.org/licenses/by/4.0/ 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 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.
spellingShingle Neuroscience
Kametani, Fuyuki
Hasegawa, Masato
Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title_full Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title_fullStr Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title_full_unstemmed Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title_short Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
title_sort reconsideration of amyloid hypothesis and tau hypothesis in alzheimer's disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5797629/
https://www.ncbi.nlm.nih.gov/pubmed/29440986
http://dx.doi.org/10.3389/fnins.2018.00025
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