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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >Human prion diseases: Molecular, cellular and population biology
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Human prion diseases: Molecular, cellular and population biology

机译：人类病毒疾病：分子，细胞和种群生物学

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The past 20 years have witnessed a dramatic resurgence of interest in a hitherto obscure neurodegenerative disease, Creutzfeldt-Jakob disease (CJD). This was driven partly by the novelty of the prion hypothesis, which sought to provide an explanation for the pathogenesis of transmissible spongiform encephalopathies, involving a unique epigenetic mechanism, and partly by events in the UK, where an outbreak of a new prion disease in cattle (bovine spongiform encephalopathy or BSE) potentially exposed a large section of the UK population to prion infectivity through a dietary route. The numbers of cases of the resultant novel disease variant CJD (vCJD), have so far been limited and peaked in the UK in the year 2000 and have subsequently declined. However, the effects of BSE and vCJD have been far-reaching. The estimated prevalence of vCJD infection in the UK is substantially higher than the numbers of clinical cases would suggest, posing a difficult dilemma for those involved in blood transfusion, tissue transplantation and cellular therapies. The clinico-pathological phenotype of human prion diseases has come under close scrutiny and molecular classification systems have been developed to account for the different diseases and their phenotypic spectra. Moreover, enhanced human and animal surveillance and better diagnostic tools have identified new human and animal prion diseases. Lastly, as the prion hypothesis has gained widespread acceptance, the concepts involved have been applied to other areas, including extra-chromosomal inheritance in fungi, long-term potentiation in memory formation and the spread of molecular pathology in diverse conditions, such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Studies at the molecular and cellular level have helped to provide a better understanding of human prion diseases, aided pathological diagnosis and helped inform public health decision-making.
机译：在过去的20年中，人们对迄今仍不清楚的神经退行性疾病Creutzfeldt-Jakob病（CJD）有了极大的兴趣。这部分是由于the病毒假说的新颖性所致，该假说旨在为可传播的海绵状脑病的发病机理提供解释，涉及独特的表观遗传机制，部分原因是在英国发生的事件，即牛中爆发了新的pr病毒病（牛海绵状脑病或牛海绵状脑病）可能通过饮食途径使英国大部分人口暴露于病毒感染。迄今为止，由此产生的新型疾病变体CJD（vCJD）的病例数量受到限制，并于2000年在英国达到顶峰，随后下降。但是，疯牛病和vCJD的影响深远。英国vCJD感染的估计患病率大大高于临床病例数，这给那些涉及输血，组织移植和细胞疗法的人带来了一个难题。人类病毒疾病的临床病理表型已经受到严格审查，并且已经开发出分子分类系统来考虑不同疾病及其表型谱。此外，加强的人类和动物监视和更好的诊断工具已经发现了新的人类和动物病毒疾病。最后，随着the病毒假说被广泛接受，所涉及的概念已应用于其他领域，包括真菌中的染色体外遗传，记忆形成的长期增强以及分子病理学在各种情况下的扩散，例如阿尔茨海默氏病，帕金森氏病和肌萎缩性侧索硬化症。在分子和细胞水平的研究有助于更好地了解人类human病毒疾病，有助于病理诊断，并有助于为公共卫生决策提供依据。

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