Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China.
Department of Pathophysiology, Key Lab of Neurological Disorder of Education, Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Curr Neuropharmacol. 2019;17(12):1146-1157. doi: 10.2174/1570159X17666190726115623.
DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eukaryotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombination, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative disorders including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD) and ataxia telangiectasia (A-T).
DNA 双链断裂（DSBs）是常见事件，被认为是真核细胞中最具毒性的损伤之一。DSBs 广泛参与许多生理过程，如 V(D)J 重组、减数分裂重组、DNA 复制和转录。在人类的多种疾病中，如神经退行性疾病，已经报道了 DSBs 的失调，需要阐明其潜在机制。在这里，我们综述了 DSB 形成和修复功能障碍的最新研究进展，这些进展有助于阐明包括阿尔茨海默病（AD）、肌萎缩侧索硬化症（ALS）、亨廷顿病（HD）和共济失调毛细血管扩张症（A-T）在内的神经退行性疾病的发病机制。
