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

Cells

Xin Xie¹  Qiuhong Hua²  Shaodeng Wang²  Junyuan Gong²  Peng Zeng²  Changsheng Du²  Ru Zhang²  Junjiang Lian²  Jiaxue Cha²  Changjie Shi²  Bowen Zhang²  Jie Lv² 

[1] CAS Key Laboratory of Receptor Research, The National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China;Shanghai Key Laboratory of Signaling and Disease Research, Laboratory of Receptor-Based Bio-Medicine, Collaborative Innovation Center for Brain Science, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China;

关键词: amyloid-β peptide;    experimental autoimmune encephalomyelitis;    multiple sclerosis;    Alzheimer’s disease;    Th17;   

DOI  :  10.3390/cells11061004

来源: DOAJ

【 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 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.

【 授权许可】

Unknown