摘要
在大多数与年龄有关的神经退行性疾病包括阿尔茨海默病(AD)中会发生神经系统的特殊蛋白的错误折叠和聚合。这种紊乱被分类为蛋白错误折叠疾病或蛋白病变,该病具有朊病毒病的主要生理生化特征。在AD病中,β淀粉样和tau蛋白、治疗老年斑的重要制剂及胞内神经纤维缠结被称作‘prionoids’,表明这些蛋白抑制朊病毒样的性质。本文中,我们描述了朊病毒样发展机制,模板化构型变化工艺诱导Aβ和tau蛋白错折和自组装;然后病原体引起的损害通过细胞与细胞间的转运进行传播,包括供体细胞中种子细胞的释放,受体和胞间转运的细胞吞噬。这种假设将为AD病提出新的治疗方案,尤其是在前期症状阶段的价值。
关键词: 阿尔茨海默病,β淀粉样肽,朊病毒样机制,tau蛋白,tans胞内繁殖,模板化构型变化
Current Alzheimer Research
Title:Prion-like Mechanisms in Alzheimer's Disease
Volume: 11 Issue: 8
Author(s): Rui-Hua Yin, Lan Tan, Teng Jiang and Jin-Tai Yu
Affiliation:
关键词: 阿尔茨海默病,β淀粉样肽,朊病毒样机制,tau蛋白,tans胞内繁殖,模板化构型变化
摘要: The misfolding and aggregation of specific proteins within nervous system occur in most age-associated neurodegenerative diseases including Alzheimer's disease (AD). This kind of disorders have been classified as the protein misfolding disease or proteopathy which share key biophysical and biochemical characteristics with prion diseases. In AD, β-amyloid (Aβ) and tau protein, capital agents for the senile plaques and intracellular neurofibrillary tangles, are called ‘prionoids’ indicating that proteins exhibit prion-like properties. In this review, we describe the prion-like mechanisms in the progression that the Aβ and tau are induced to misfold and self-assemble by a process of templated conformational change and then the lesion caused by the pathogenic agents spread out through the cell-to-cell transportation, including release of intracellular seeds by the donor cell, cellular uptake by the recipient and intercellular transport. This hypothesis will suggest new therapeutic strategies for AD, especially valuable in the pre-symptomatic phase.
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Cite this article as:
Rui-Hua Yin, Lan Tan, Teng Jiang and Yu Jin-Tai, Prion-like Mechanisms in Alzheimer's Disease, Current Alzheimer Research 2014; 11 (8) . https://dx.doi.org/10.2174/156720501108140910121425
DOI https://dx.doi.org/10.2174/156720501108140910121425 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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