摘要
积累的DNA损伤和损伤DNA修复系统参与不同的神经退行性疾病的发病机制。当DNA损伤太广泛,DNA损伤反应途径触发了细胞衰老或凋亡。然而,DNA损伤增加的水平是否在神经退行性疾病中是神经退行性的事件的原因而不是结果还有待建立。在可能的DNA损伤、DNA双链断裂(双边带)是罕见的事,然而它们是最致命的形式的DNA损伤。在神经元中,双边带尤其有害,因为它们比增殖细胞的DNA修复能力更低。 在这里,我们提供双边带修复系统的描述和形容人类研究显示几种类型的DNA损伤的存在主要在三个神经退行性疾病,包括阿尔茨海默病(AD)、帕金森病(PD)和亨廷顿氏病(HD)。然后,我们分析双边带的作用缺乏积累和双边带修复系统的神经退化通过研究神经退行性疾病的动物模型来检查。
关键词: 阿尔茨海默氏症、DNA损伤、DNA修复、DNA双链断裂、亨廷顿氏舞蹈症、神经退行性疾病、帕金森病。
Current Alzheimer Research
Title:DNA Double Strand Breaks: A Common Theme in Neurodegenerative Diseases
Volume: 13 Issue: 11
Author(s): Daniela Merlo, Cristiana Mollinari, Mauro Racaniello, Enrico Garaci, Alessio Cardinale
Affiliation:
关键词: 阿尔茨海默氏症、DNA损伤、DNA修复、DNA双链断裂、亨廷顿氏舞蹈症、神经退行性疾病、帕金森病。
摘要: Accumulation of DNA damage and impairment of DNA repair systems are involved in the pathogenesis of different neurodegenerative diseases. Whenever DNA damage is too extensive, the DNA damage response pathway provides for triggering cellular senescence and/or apoptosis. However, whether the increased level of DNA damage in neurodegenerative disorders is a cause rather than the consequence of neurodegenerative events remains to be established. Among possible DNA lesions, DNA double strand breaks (DSBs) are rare events, nevertheless they are the most lethal form of DNA damage. In neurons, DSBs are particularly deleterious because of their reduced DNA repair capability as compared to proliferating cells.
Here, we provide a description of DSB repair systems and describe human studies showing the presence of several types of DNA lesions in three major neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Then, we analyze the role of DSB accumulation and deficiency of DSB repair systems in neurodegeneration by examining studies on animal models of neurodegenerative diseases.
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Cite this article as:
Daniela Merlo, Cristiana Mollinari, Mauro Racaniello, Enrico Garaci, Alessio Cardinale , DNA Double Strand Breaks: A Common Theme in Neurodegenerative Diseases, Current Alzheimer Research 2016; 13 (11) . https://dx.doi.org/10.2174/1567205013666160401114915
DOI https://dx.doi.org/10.2174/1567205013666160401114915 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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