Abstract |
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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Authors | Masaaki Waragai, Gilbert Ho, Yoshiki Takamatsu, Ryoko Wada, Shuei Sugama, Takato Takenouchi, Eliezer Masliah, Makoto Hashimoto |
Journal | Journal of Alzheimer's disease : JAD
(J Alzheimers Dis)
Vol. 76
Issue 4
Pg. 1249-1253
( 2020)
ISSN: 1875-8908 [Electronic] Netherlands |
PMID | 32623396
(Publication Type: Journal Article)
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Chemical References |
- ADIPOQ protein, human
- Adiponectin
- Amyloid beta-Peptides
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Topics |
- Adiponectin
(metabolism)
- Aging
(physiology)
- Alzheimer Disease
(drug therapy)
- Amyloid beta-Peptides
(metabolism)
- Brain
(metabolism)
- Humans
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