PDF(Pubmed)
Abstract：
Neurodegeneration is becoming one of the leading causes of death worldwide as the population expands and grows older. There is a growing desire to understand the mechanisms behind prion proteins as well as the prion-like proteins that make up neurodegenerative diseases (NDs), including Alzheimer\'s disease (AD) and Parkinson\'s disease (PD). Both amyloid-β (Aβ) and hyperphosphorylated tau (p-tau) proteins behave in ways similar to those of the infectious form of the prion protein, PrPSc, such as aggregating, seeding, and replicating under not yet fully understood mechanisms, thus the designation of prion-like. This review aims to highlight the shared mechanisms between prion-like proteins and prion proteins in the structural variations associated with aggregation and disease development. These mechanisms largely focus on the dysregulation of protein homeostasis, self-replication, and protein aggregation, and this knowledge could contribute to diagnoses and treatments for the given NDs.
摘要：
随着人口的增长和年龄的增长，神经变性正在成为世界范围内死亡的主要原因之一。人们越来越希望了解朊病毒蛋白以及构成神经退行性疾病（ND）的朊病毒样蛋白背后的机制，包括阿尔茨海默病(AD)和帕金森病(PD)。淀粉样蛋白-β（Aβ）和高磷酸化tau（p-tau）蛋白的行为方式与朊病毒蛋白的感染形式相似，PrPSc,例如聚合，播种,并在尚未完全理解的机制下复制，因此被指定为病毒样。这篇综述旨在强调朊病毒样蛋白和朊病毒蛋白在与聚集和疾病发展相关的结构变异中的共同机制。这些机制主要集中在蛋白质稳态的失调，自我复制,和蛋白质聚集，这些知识可能有助于对给定的ND进行诊断和治疗。
