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Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ

Emerging data have highlighted the coexistence of multiple sclerosis (MS) and Alzheimer’s disease (AD), both of which are common central nervous system degenerative diseases with a heavy burden on patients, their families, and society. However, it is unclear how MS progresses under an AD pathologica...

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Autores principales: Shi, Changjie, Cha, Jiaxue, Gong, Junyuan, Wang, Shaodeng, Zeng, Peng, Lian, Junjiang, Zhang, Bowen, Hua, Qiuhong, Lv, Jie, Du, Changsheng, Xie, Xin, Zhang, Ru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8946952/
https://www.ncbi.nlm.nih.gov/pubmed/35326455
http://dx.doi.org/10.3390/cells11061004
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author Shi, Changjie
Cha, Jiaxue
Gong, Junyuan
Wang, Shaodeng
Zeng, Peng
Lian, Junjiang
Zhang, Bowen
Hua, Qiuhong
Lv, Jie
Du, Changsheng
Xie, Xin
Zhang, Ru
author_facet Shi, Changjie
Cha, Jiaxue
Gong, Junyuan
Wang, Shaodeng
Zeng, Peng
Lian, Junjiang
Zhang, Bowen
Hua, Qiuhong
Lv, Jie
Du, Changsheng
Xie, Xin
Zhang, Ru
author_sort Shi, Changjie
collection PubMed
description Emerging data have highlighted the coexistence of multiple sclerosis (MS) and Alzheimer’s disease (AD), both of which are common central nervous system degenerative diseases with a heavy burden on patients, their families, and society. However, it is unclear how MS progresses under an AD pathological background. We aimed to address the question of how MS progresses under an AD pathological background. We induced the experimental autoimmune encephalomyelitis (EAE) model of MS in two types of AD mouse models, Tg6799 and APP/PS1 mice. We found that, compared with wild-type mice, the clinical symptoms of EAE were significantly ameliorated in APP/PS1 mice but not in Tg6799 mice. Moreover, a much lower level of serum Aβ was observed in Tg6799 mice. EAE clinical symptoms in Tg6799 and C57BL/6J mice were ameliorated by intraperitoneal injection of Aβ42. Peripheral administration of Aβ42 peptides was able to inhibit Th17 development in vivo, which is likely to occur through the inhibition of IL-6 production in dendritic cells. Our findings revealed that AD and EAE could coexist in the same mouse, and Aβ residing in peripheral circulation likely plays an anti-inflammatory role in preventing EAE progression. These findings reveal the potential benefit of Aβ, one of the supervillains of AD, at least in certain contexts.
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spelling pubmed-89469522022-03-25 Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ Shi, Changjie Cha, Jiaxue Gong, Junyuan Wang, Shaodeng Zeng, Peng Lian, Junjiang Zhang, Bowen Hua, Qiuhong Lv, Jie Du, Changsheng Xie, Xin Zhang, Ru Cells Article Emerging data have highlighted the coexistence of multiple sclerosis (MS) and Alzheimer’s disease (AD), both of which are common central nervous system degenerative diseases with a heavy burden on patients, their families, and society. However, it is unclear how MS progresses under an AD pathological background. We aimed to address the question of how MS progresses under an AD pathological background. We induced the experimental autoimmune encephalomyelitis (EAE) model of MS in two types of AD mouse models, Tg6799 and APP/PS1 mice. We found that, compared with wild-type mice, the clinical symptoms of EAE were significantly ameliorated in APP/PS1 mice but not in Tg6799 mice. Moreover, a much lower level of serum Aβ was observed in Tg6799 mice. EAE clinical symptoms in Tg6799 and C57BL/6J mice were ameliorated by intraperitoneal injection of Aβ42. Peripheral administration of Aβ42 peptides was able to inhibit Th17 development in vivo, which is likely to occur through the inhibition of IL-6 production in dendritic cells. Our findings revealed that AD and EAE could coexist in the same mouse, and Aβ residing in peripheral circulation likely plays an anti-inflammatory role in preventing EAE progression. These findings reveal the potential benefit of Aβ, one of the supervillains of AD, at least in certain contexts. MDPI 2022-03-16 /pmc/articles/PMC8946952/ /pubmed/35326455 http://dx.doi.org/10.3390/cells11061004 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Shi, Changjie
Cha, Jiaxue
Gong, Junyuan
Wang, Shaodeng
Zeng, Peng
Lian, Junjiang
Zhang, Bowen
Hua, Qiuhong
Lv, Jie
Du, Changsheng
Xie, Xin
Zhang, Ru
Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title_full Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title_fullStr Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title_full_unstemmed Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title_short Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ
title_sort amelioration of experimental autoimmune encephalomyelitis in alzheimer’s disease mouse models: a potential role for aβ
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8946952/
https://www.ncbi.nlm.nih.gov/pubmed/35326455
http://dx.doi.org/10.3390/cells11061004
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