Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for A beta
文献类型：期刊论文
| 作者 | Shi, Changjie1; Cha, Jiaxue1; Gong, Junyuan1; Wang, Shaodeng1; Zeng, Peng1; Lian, Junjiang1; Zhang, Bowen1; Hua, Qiuhong1; Lv, Jie1; Du, Changsheng1 |
| 刊名 | CELLS
 |
| 出版日期 | 2022-03-01 |
| 卷号 | 11期号:6页码:11 |
| 关键词 | amyloid-beta peptide experimental autoimmune encephalomyelitis multiple sclerosis Alzheimer's disease Th17 |
| DOI | 10.3390/cells11061004 |
| 通讯作者 | Zhang, Ru(ru.zhang@tongji.edu.cn) |
| 英文摘要 | 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 A beta was observed in Tg6799 mice. EAE clinical symptoms in Tg6799 and C57BL/6J mice were ameliorated by intraperitoneal injection of A beta 42. Peripheral administration of A beta 42 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 A beta residing in peripheral circulation likely plays an anti-inflammatory role in preventing EAE progression. These findings reveal the potential benefit of A beta, one of the supervillains of AD, at least in certain contexts. |
| WOS关键词 | AMYLOID PRECURSOR PROTEIN ; PEPTIDE ; PATHOGENESIS ; MUTATIONS ; PATHOLOGY ; CELLS |
| 资助项目 | Ministry of Science and Technology of China[2017YFA0104002] |
| WOS研究方向 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000775607400001 |
| 出版者 | MDPI |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/299970]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Zhang, Ru |
| 作者单位 | 1.Tongji Univ, Collaborat Innovat Ctr Brain Sci, Sch Life Sci & Technol, Shanghai Key Lab Signaling & Dis Res,Lab Receptor, Shanghai 200092, Peoples R China 2.Chinese Acad Sci, Natl Ctr Drug Screening, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Shi, Changjie,Cha, Jiaxue,Gong, Junyuan,et al. Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for A beta[J]. CELLS,2022,11(6):11. |
| APA | Shi, Changjie.,Cha, Jiaxue.,Gong, Junyuan.,Wang, Shaodeng.,Zeng, Peng.,...&Zhang, Ru.(2022).Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for A beta.CELLS,11(6),11. |
| MLA | Shi, Changjie,et al."Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for A beta".CELLS 11.6(2022):11. |
入库方式： OAI收割
来源：上海药物研究所
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