视网膜是中枢神经系统的一部分。在胚胎起源上，视网膜和大脑均由神经管发育而来。因此，许多发生在大脑的神经退行性疾病往往会同时累及视网膜。而神经退行性疾病过程中相关的特征性病理改变，如病理性蛋白聚集和神经血管单元破坏也常能在视网膜组织中被检测到。在一些神经退行性疾病中，眼部的病理改变甚至在临床症状出现之前就已发生；其次视网膜易于观察且局部治疗操作便捷，因此近年来视网膜在中枢神经退行性疾病发病机制研究、早期诊断和新型治疗方式探究等方面备受关注。该文对常见神经退行性疾病的眼部病理改变进行综述，旨在为大脑和视网膜神经退行疾病的发病机制、诊断以及治疗研究提供新的见解。

The retina is a part of the central nervous system. Developmentally, both retina and brain are derived from the neural tube. Therefore, many neurodegenerative diseases that occur in the brain tend to involve both the retina. In the process of neurodegenerative diseases, related characteristic pathological changes, such as pathological protein aggregation, neurovascular unit impairment can often be detected in retinal tissue. In some neurodegenerative diseases, pathological changes in the eye occur even before clinical symptoms appear. In addition, the retina are easy to observe and local treatments are convenient. In recent years, the manifestations of the retina have attracted much attention in the study of pathogenesis, early diagnosis, and new treatments of systemic central neurodegenerative diseases. In this way, this article reviews the ocular pathological changes of common neurodegenerative diseases, aiming to provide new insights into the pathogenesis, diagnosis, and treatment of brain and retinal neurodegenerative diseases.

外伤性视神经病变是因外力损伤视神经，进而严重损害视力的致盲性眼病。自噬是一种细胞内降解途径，有助于维持细胞正常组分合成与受损细胞器及有毒细胞成分的分解之间的平衡。视神经受创后，视神经和视网膜中自噬标志物增加。自噬在外伤性视神经病变的不同阶段对视网膜神经节细胞可能起不同作用。多数研究表明，上调自噬可以减轻外伤性视神经病变中视网膜神经节细胞的死亡；也有研究提示在视神经损伤后极早的时期抑制自噬可以抑制视网膜神经节细胞轴突变性。该文对自噬的定义及功能、自噬的发生机制、视神经创伤后自噬水平改变、自噬在视神经创伤后对视网膜神经节细胞的作用的研究结果进行综述。

Traumatic optic neuropathy is a blinding eye disease that causes severe damage to vision due to external force damage to the optic nerve.. Autophagy is an intracellular degradation pathway that helps maintain the balance between the synthesis

of normal cell components and the breakdown of damaged organelles and toxic cellular components. Autophagy markers are increased in optic nerve and retina after optic nerve trauma. Autophagy may play different roles on retinal ganglion cells (RGCs) at different stages of traumatic optic neuropathy. Most studies have shown that upregulating autophagy can attenuate RGCs death in traumatic optic neuropathy; however, it has also been suggested that inhibition of autophagy at ultra-early stage after injury can inhibit RGCs axonal degeneration. In this review, we reviewed the definition and function of autophagy, the mechanism of autophagy, and summarized the change of autophagy level after optic nerve trauma, as well as the effects of autophagy in RGCs after optic nerve trauma.