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Published on: March 16, 2016
Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer's Disease Mouse Models: A Potential Role for
Changjie Shi1, Jiaxue Cha1, Junyuan Gong1
1Shanghai 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.
Abstract:
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.
Insights
Alzheimer's disease (AD) pathology may protect against multiple sclerosis (MS) progression. Amyloid-beta (Aβ) peptides in the blood appear to reduce inflammation, potentially benefiting MS patients.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Multiple sclerosis (MS) and Alzheimer's disease (AD) are common CNS degenerative diseases.
- The interaction and progression of MS under AD pathology are not well understood.
Purpose of the Study:
- To investigate how MS progresses in the context of AD pathology.
- To explore the role of amyloid-beta (Aβ) in modulating MS progression.
Main Methods:
- Induced experimental autoimmune encephalomyelitis (EAE), an MS model, in AD mouse models (Tg6799 and APP/PS1).
- Administered Aβ42 peptides peripherally to assess effects on EAE.
- Measured clinical symptoms and inflammatory markers (IL-6, Th17).
Main Results:
- EAE symptoms were ameliorated in APP/PS1 mice but not Tg6799 mice compared to wild-type.
- Tg6799 mice exhibited lower serum Aβ levels.
- Peripheral Aβ42 injection ameliorated EAE symptoms by inhibiting Th17 development via reduced IL-6 production in dendritic cells.
Conclusions:
- AD and EAE can coexist within the same organism.
- Peripheral Aβ may possess anti-inflammatory properties, potentially inhibiting MS progression.
- Amyloid-beta, often implicated in AD, might offer protective benefits in certain inflammatory contexts.
