Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans

Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the...

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Autores principales: Shuju Bai, Wenbo Wang, Zhiwei Zhang, Mengyao Li, Zehan Chen, Jiuqiao Wang, Yanlin Zhao, Lu An, Yuxiang Wang, Shu Xing, Xueqi Fu, Junfeng Ma
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/42ab69ae05c44253a7522b8e91b06038
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spelling oai:doaj.org-article:42ab69ae05c44253a7522b8e91b060382021-11-12T05:16:57ZEthanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans1663-436510.3389/fnagi.2021.762659https://doaj.org/article/42ab69ae05c44253a7522b8e91b060382021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fnagi.2021.762659/fullhttps://doaj.org/toc/1663-4365Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the lifespan of Caenorhabiditis elegans in a previous study. Based on that study, we tested the effect of ethanol on Alzheimer’s disease transgenic Caenorhabiditis elegans strain CL4176, which expresses amyloid-β1-42 peptide in body wall muscle cells. Ethanol delayed paralysis and reduced amyloid-β oligomers in Caenorhabiditis elegans worms of the CL4176 strain. Moreover, ethanol could induce the nuclear translocation of DAF-16 in the nematodes. However, in worms that were fed daf-16 RNAi bacteria, ethanol no longer delayed the paralysis. The qPCR assays showed that ethanol increases the expression of daf-16, hsf-1 and their common target genes- small heat shock protein genes. In addition, we also found that ethanol could increase lysosome mass in the CL4176 worms. In summary, our study indicated that ethanol attenuated amyloid-β toxicity in the Alzheimer’s disease model of Caenorhabiditis elegans via increasing the level of lysosomes to promote amyloid-β degradation and upregulating the levels of small heat shock protein genes to reduce amyloid-β aggregation.Shuju BaiWenbo WangZhiwei ZhangMengyao LiZehan ChenJiuqiao WangYanlin ZhaoLu AnYuxiang WangShu XingXueqi FuXueqi FuJunfeng MaJunfeng MaFrontiers Media S.A.articleAlzheimer’s diseaseamyloid-βCaenorhabiditis elegansethanolDAF-16lysosomeNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENFrontiers in Aging Neuroscience, Vol 13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Alzheimer’s disease
amyloid-β
Caenorhabiditis elegans
ethanol
DAF-16
lysosome
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
spellingShingle Alzheimer’s disease
amyloid-β
Caenorhabiditis elegans
ethanol
DAF-16
lysosome
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Shuju Bai
Wenbo Wang
Zhiwei Zhang
Mengyao Li
Zehan Chen
Jiuqiao Wang
Yanlin Zhao
Lu An
Yuxiang Wang
Shu Xing
Xueqi Fu
Xueqi Fu
Junfeng Ma
Junfeng Ma
Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
description Amyloid-β, a hallmark of Alzheimer’s disease, forms toxic intracellular oligomers and extracellular senile plaques resulting in neuronal toxicity. Ethanol is widely consumed worldwide. Moderate ethanol consumption has numerous benefits in humans. We found that ethanol could significantly extend the lifespan of Caenorhabiditis elegans in a previous study. Based on that study, we tested the effect of ethanol on Alzheimer’s disease transgenic Caenorhabiditis elegans strain CL4176, which expresses amyloid-β1-42 peptide in body wall muscle cells. Ethanol delayed paralysis and reduced amyloid-β oligomers in Caenorhabiditis elegans worms of the CL4176 strain. Moreover, ethanol could induce the nuclear translocation of DAF-16 in the nematodes. However, in worms that were fed daf-16 RNAi bacteria, ethanol no longer delayed the paralysis. The qPCR assays showed that ethanol increases the expression of daf-16, hsf-1 and their common target genes- small heat shock protein genes. In addition, we also found that ethanol could increase lysosome mass in the CL4176 worms. In summary, our study indicated that ethanol attenuated amyloid-β toxicity in the Alzheimer’s disease model of Caenorhabiditis elegans via increasing the level of lysosomes to promote amyloid-β degradation and upregulating the levels of small heat shock protein genes to reduce amyloid-β aggregation.
format article
author Shuju Bai
Wenbo Wang
Zhiwei Zhang
Mengyao Li
Zehan Chen
Jiuqiao Wang
Yanlin Zhao
Lu An
Yuxiang Wang
Shu Xing
Xueqi Fu
Xueqi Fu
Junfeng Ma
Junfeng Ma
author_facet Shuju Bai
Wenbo Wang
Zhiwei Zhang
Mengyao Li
Zehan Chen
Jiuqiao Wang
Yanlin Zhao
Lu An
Yuxiang Wang
Shu Xing
Xueqi Fu
Xueqi Fu
Junfeng Ma
Junfeng Ma
author_sort Shuju Bai
title Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
title_short Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
title_full Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
title_fullStr Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
title_full_unstemmed Ethanol Alleviates Amyloid-β-Induced Toxicity in an Alzheimer’s Disease Model of Caenorhabiditis elegans
title_sort ethanol alleviates amyloid-β-induced toxicity in an alzheimer’s disease model of caenorhabiditis elegans
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/42ab69ae05c44253a7522b8e91b06038
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