The ME7 prion model of neurodegeneration as a tool to understand and target neuroinflammation in Alzheimer’s disease

Q3 Pharmacology, Toxicology and Pharmaceutics
Joe K. Chouhan , Susan B. Fowler , Carl I. Webster , Jessica L. Teeling
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引用次数: 4

Abstract

To develop disease-modifying therapies for Alzheimer’s disease (AD), an understanding of the pathways that lead to synaptic damage and neuronal cell death is required. The ME7 prion mouse model shares hallmarks of human neurodegenerative diseases and has a well-defined disease progression that can be monitored non-invasively through changes in behaviour. In addition, a strong involvement of neuroinflammation in ME7 disease progression and systemic inflammatory challenge has provided rationale to study and target cytokines in human AD patients. Furthermore, susceptibility of the model to acute cognitive deficits generated a model of delirium has supported human dementia studies. Thus, the ME7 prion model provides a translatable model of neurodegeneration and neuroinflammation that could provide validation of potential treatments against the inflammatory response during neurodegeneration.

Abstract Image

神经退行性变的ME7朊病毒模型作为了解和靶向阿尔茨海默病神经炎症的工具
为了开发阿尔茨海默病(AD)的疾病修饰疗法,需要了解导致突触损伤和神经元细胞死亡的途径。ME7朊病毒小鼠模型具有人类神经退行性疾病的特征,并且具有明确的疾病进展,可以通过行为变化非侵入性地监测。此外,神经炎症在ME7疾病进展和全身炎症挑战中的强烈参与为研究和靶向人类AD患者的细胞因子提供了理论依据。此外,该模型对急性认知缺陷的易感性产生了谵妄模型,支持了人类痴呆症的研究。因此,ME7朊病毒模型提供了一个可翻译的神经变性和神经炎症模型,可以为神经变性期间对抗炎症反应的潜在治疗提供验证。
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来源期刊
Drug Discovery Today: Disease Models
Drug Discovery Today: Disease Models Pharmacology, Toxicology and Pharmaceutics-Drug Discovery
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期刊介绍: Drug Discovery Today: Disease Models discusses the non-human experimental models through which inference is drawn regarding the molecular aetiology and pathogenesis of human disease. It provides critical analysis and evaluation of which models can genuinely inform the research community about the direct process of human disease, those which may have value in basic toxicology, and those which are simply designed for effective expression and raw characterisation.
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