Neurodegenerative diseases (NDs) are one of the major health threats to human characterized by selective and progressive neuronal loss. The mechanisms of NDs are still not fully understood. The study of genetic defects and disease-related proteins offers us a window into the mystery of it, and the extension of knowledge indicates that different NDs share similar features, mechanisms, and even genetic or protein abnormalities. Among these findings, PARK7 and its production DJ-1 protein, which was initially found implicated in PD, have also been found altered in other NDs. PARK7 mutations, altered expression and posttranslational modification (PTM) cause DJ-1 abnormalities, which in turn lead to downstream mechanisms shared by most NDs, such as mitochondrial dysfunction, oxidative stress, protein aggregation, autophagy defects, and so on. The knowledge of DJ-1 derived from PD researches might apply to other NDs in both basic research and clinical application, and might yield novel insights into and alternative approaches for dealing with NDs.

神经退行性疾病 (NDs) 是人类面临的主要健康威胁之一，其特征是选择性和进行性神经元丢失。ND的机制仍未完全了解。对遗传缺陷和疾病相关蛋白的研究为我们提供了一扇了解其奥秘的窗口，知识的扩展表明不同的NDs具有相似的特征、机制，甚至遗传或蛋白质异常。在这些发现中，最初发现与 PD 相关的PARK7及其产生的 DJ-1 蛋白也被发现在其他 ND 中发生了改变。公园7突变、表达改变和翻译后修饰（PTM）导致DJ-1异常，进而导致大多数NDs共有的下游机制，如线粒体功能障碍、氧化应激、蛋白质聚集、自噬缺陷等。来自 PD 研究的 DJ-1 知识可能适用于基础研究和临床应用中的其他 ND，并可能为处理 ND 产生新的见解和替代方法。