Deng Lan, Li Yuanyuan, Sha Ailong
School of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing, 404120, China.
School of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing, 404120, China; School of Teacher Education, Chongqing Three Gorges University, Chongqing, 404120, China.
Microb Pathog. 2025 Sep;206:107789. doi: 10.1016/j.micpath.2025.107789. Epub 2025 Jun 4.
In recent years, important progress has been made in the study of the pathogenesis of neurodegenerative diseases, especially the role of protein misfolding and aberrant aggregation in the development of diseases has attracted much attention. As a class of zoonotic infectious neurodegenerative diseases caused by prion protein misfolding and aggregation, prion diseases, with their unique transmission characteristics, have provided important insights for the study of other neurodegenerative diseases. A growing body of research has shown that similar abnormal protein aggregation phenomena occur in common neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). These misfolded proteins exhibit striking similarities to prions in terms of seeding capacity, cytotoxicity, and propagation properties. Further investigation into the prion-like behavior of these aberrant proteins in neurodegenerative diseases can offer new directions for diagnosis and treatment. Recent studies have demonstrated that AD can be transmitted through medical routes, which warns us that neurodegenerative diseases are potentially infectious and deserve further attention and research. This article systematically reviews the pathological features and transmission mechanisms of abnormal proteins in prion diseases and other neurodegenerative disorders, aiming to provide a new perspective for the prevention and treatment of these diseases. Moreover, this research holds significant implications for public health and clinical practice. By revealing the potential transmissibility of neurodegenerative diseases, it can help improve medical protocols and reduce the risk of iatrogenic transmission.
近年来，神经退行性疾病发病机制的研究取得了重要进展，尤其是蛋白质错误折叠和异常聚集在疾病发展中的作用备受关注。作为一类由朊病毒蛋白错误折叠和聚集引起的人畜共患传染性神经退行性疾病，朊病毒疾病以其独特的传播特征，为其他神经退行性疾病的研究提供了重要见解。越来越多的研究表明，在阿尔茨海默病（AD）和帕金森病（PD）等常见神经退行性疾病中也会出现类似的异常蛋白聚集现象。这些错误折叠的蛋白在种子形成能力、细胞毒性和传播特性方面与朊病毒表现出惊人的相似性。进一步研究这些异常蛋白在神经退行性疾病中的类朊病毒行为可为诊断和治疗提供新方向。最近的研究表明，AD可通过医源性途径传播，这警示我们神经退行性疾病具有潜在传染性，值得进一步关注和研究。本文系统综述了朊病毒疾病和其他神经退行性疾病中异常蛋白的病理特征和传播机制，旨在为这些疾病的防治提供新视角。此外，本研究对公共卫生和临床实践具有重要意义。通过揭示神经退行性疾病的潜在传播性，有助于改进医疗规程并降低医源性传播风险。
