Neurodegenerative disorders like Parkinson's disease, Alzheimer's disease, or amyotrophic lateral sclerosis are affecting a rapidly increasing population worldwide. While common pathomechanisms such as protein aggregation, axonal degeneration, dysfunction of protein clearing and an altered immune response have been characterized, no disease-modifying therapies have been developed so far. Interestingly, a significant involvement of the Rho kinase (ROCK) signaling pathway has been described in all of these mechanisms making it a promising target for new therapeutic approaches.

In this article, we first review current knowledge of the involvement of ROCK in neurodegenerative disorders and the utility of its inhibition as a disease-modifying therapy in different neurodegenerative disorders. After a detailed description of the biochemical characteristics of ROCK and its molecular interactors, differences of ROCK-expression under physiological and pathological conditions are compared. Next, different pharmacological and molecular-genetic strategies to inhibit ROCK-function are discussed, focusing on pharmacological ROCK-inhibitors. The role of the ROCK-pathway in cellular processes that are central in neurodegenerative disorders pathology like axonal degeneration, autophagy, synaptic and glial function is explained in detail. Finally, all available data on ROCK-inhibition in different animal models of neurodegenerative disorders is reviewed and first approaches for translation into human patients are discussed.

Taken together, there is now extensive evidence from preclinical studies in several neurodegenerative disorders that characterize ROCK as a promising drug target for further translational research in neurodegenerative disorders.

帕金森氏病，阿尔茨海默氏病或​​肌萎缩性侧索硬化症等神经退行性疾病正在影响全球范围内迅速增长的人口。尽管已经表征了常见的病理机制，如蛋白质聚集，轴突变性，蛋白质清除功能障碍和免疫反应改变，但迄今为止，尚未开发出任何改善疾病的疗法。有趣的是，已经在所有这些机制中描述了Rho激酶（ROCK）信号通路的重要参与，使其成为新治疗方法的有希望的靶标。

在本文中，我们首先回顾了ROCK在神经退行性疾病中的作用及其抑制作用在不同神经退行性疾病中作为疾病改良疗法的实用性的当前知识。在详细描述了ROCK及其分子相互作用物的生化特性之后，比较了ROCK在生理和病理条件下的表达差异。接下来，讨论了抑制ROCK功能的不同药理和分子遗传学策略，重点是药理学ROCK抑制剂。详细解释了ROCK途径在神经退行性疾病病理学（如轴突变性，自噬，突触和神经胶质功能）中至关重要的细胞过程中的作用。最后，

综上所述，现在在一些神经退行性疾病的临床前研究中获得了广泛的证据，这些证据将ROCK表征为神经退行性疾病的进一步转化研究的有希望的药物靶标。