Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease

Despite the apparent neurotoxicity of amyloid-β (Aβ), recent clinical trials of Aβ immunotherapy have not shown any clinical benefit in Alzheimer’s disease (AD). Given this, clarification of the next generation therapeutic strategy in AD is warranted. Hypothetically, adiponectin might be involved in...

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Autores principales: Waragai, Masaaki, Ho, Gilbert, Takamatsu, Yoshiki, Wada, Ryoko, Sugama, Shuei, Takenouchi, Takato, Masliah, Eliezer, Hashimoto, Makoto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: IOS Press 2020
Materias:
Commentary
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504987/
https://www.ncbi.nlm.nih.gov/pubmed/32623396
http://dx.doi.org/10.3233/JAD-200416
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author Waragai, Masaaki
Ho, Gilbert
Takamatsu, Yoshiki
Wada, Ryoko
Sugama, Shuei
Takenouchi, Takato
Masliah, Eliezer
Hashimoto, Makoto
author_facet Waragai, Masaaki
Ho, Gilbert
Takamatsu, Yoshiki
Wada, Ryoko
Sugama, Shuei
Takenouchi, Takato
Masliah, Eliezer
Hashimoto, Makoto
author_sort Waragai, Masaaki
collection PubMed
description Despite the apparent neurotoxicity of amyloid-β (Aβ), recent clinical trials of Aβ immunotherapy have not shown any clinical benefit in Alzheimer’s disease (AD). Given this, clarification of the next generation therapeutic strategy in AD is warranted. Hypothetically, adiponectin might be involved in promoting amyloidogenic evolvability in reproduction, which may result in the adiponectin paradox through antagonistic pleiotropy mechanism in aging, leading to AD. Accordingly, preventing the adiponectin paradox by suppressing adiponectin signaling might prove therapeutic in AD.
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spelling pubmed-75049872020-10-06 Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease Waragai, Masaaki Ho, Gilbert Takamatsu, Yoshiki Wada, Ryoko Sugama, Shuei Takenouchi, Takato Masliah, Eliezer Hashimoto, Makoto J Alzheimers Dis Commentary Despite the apparent neurotoxicity of amyloid-β (Aβ), recent clinical trials of Aβ immunotherapy have not shown any clinical benefit in Alzheimer’s disease (AD). Given this, clarification of the next generation therapeutic strategy in AD is warranted. Hypothetically, adiponectin might be involved in promoting amyloidogenic evolvability in reproduction, which may result in the adiponectin paradox through antagonistic pleiotropy mechanism in aging, leading to AD. Accordingly, preventing the adiponectin paradox by suppressing adiponectin signaling might prove therapeutic in AD. IOS Press 2020-08-18 /pmc/articles/PMC7504987/ /pubmed/32623396 http://dx.doi.org/10.3233/JAD-200416 Text en © 2020 – IOS Press and the authors. All rights reserved https://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License (https://creativecommons.org/licenses/by-nc/4.0/) , which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Waragai, Masaaki
Ho, Gilbert
Takamatsu, Yoshiki
Wada, Ryoko
Sugama, Shuei
Takenouchi, Takato
Masliah, Eliezer
Hashimoto, Makoto
Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title_full Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title_fullStr Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title_full_unstemmed Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title_short Adiponectin Paradox as a Therapeutic Target in Alzheimer’s Disease
title_sort adiponectin paradox as a therapeutic target in alzheimer’s disease
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504987/
https://www.ncbi.nlm.nih.gov/pubmed/32623396
http://dx.doi.org/10.3233/JAD-200416
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