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Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease

This present study examined the effect of Tamibarotene (AM80) in APP/PS1 mice, a well-established AD mouse model. AM80 was intraperitoneal administered to 3-month-old APP/PS1 mice at a dose of 5 mg/kg/day for 16 weeks. The results clearly showed that AM80 could reduce amyloid-β peptides through impa...

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Detalles Bibliográficos
Autores principales: Qiao, Aimin, Li, Jieyi, Hu, Yaohua, Wang, Jinquan, Zhao, Zizhuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019995/
https://www.ncbi.nlm.nih.gov/pubmed/33842919
http://dx.doi.org/10.1016/j.ibneur.2021.02.004
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author Qiao, Aimin
Li, Jieyi
Hu, Yaohua
Wang, Jinquan
Zhao, Zizhuo
author_facet Qiao, Aimin
Li, Jieyi
Hu, Yaohua
Wang, Jinquan
Zhao, Zizhuo
author_sort Qiao, Aimin
collection PubMed
description This present study examined the effect of Tamibarotene (AM80) in APP/PS1 mice, a well-established AD mouse model. AM80 was intraperitoneal administered to 3-month-old APP/PS1 mice at a dose of 5 mg/kg/day for 16 weeks. The results clearly showed that AM80 could reduce amyloid-β peptides through impact on APP processing and reduce microglia and astrocyte activation in APP/PS1 mice. The most notable finding in the present study was that inhibitory effect on BACE1 mediated by NF-κB pathway underlies the anti-inflammatory action of AM80. Moreover, AM80 could significantly decrease synaptic loss and enhance the expressions of Synapsin and Drebrin. Therefore, AM80 treatment may have the preclinical prevention of AD with new therapeutic strategies.
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spelling pubmed-80199952021-04-08 Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease Qiao, Aimin Li, Jieyi Hu, Yaohua Wang, Jinquan Zhao, Zizhuo IBRO Neurosci Rep Research Paper This present study examined the effect of Tamibarotene (AM80) in APP/PS1 mice, a well-established AD mouse model. AM80 was intraperitoneal administered to 3-month-old APP/PS1 mice at a dose of 5 mg/kg/day for 16 weeks. The results clearly showed that AM80 could reduce amyloid-β peptides through impact on APP processing and reduce microglia and astrocyte activation in APP/PS1 mice. The most notable finding in the present study was that inhibitory effect on BACE1 mediated by NF-κB pathway underlies the anti-inflammatory action of AM80. Moreover, AM80 could significantly decrease synaptic loss and enhance the expressions of Synapsin and Drebrin. Therefore, AM80 treatment may have the preclinical prevention of AD with new therapeutic strategies. Elsevier 2021-02-14 /pmc/articles/PMC8019995/ /pubmed/33842919 http://dx.doi.org/10.1016/j.ibneur.2021.02.004 Text en © 2021 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Paper
Qiao, Aimin
Li, Jieyi
Hu, Yaohua
Wang, Jinquan
Zhao, Zizhuo
Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title_full Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title_fullStr Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title_full_unstemmed Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title_short Reduction BACE1 expression via suppressing NF-κB mediated signaling by Tamibarotene in a mouse model of Alzheimer’s disease
title_sort reduction bace1 expression via suppressing nf-κb mediated signaling by tamibarotene in a mouse model of alzheimer’s disease
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019995/
https://www.ncbi.nlm.nih.gov/pubmed/33842919
http://dx.doi.org/10.1016/j.ibneur.2021.02.004
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