The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease.
The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease.
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DOI：
10.1155/2016/3619274
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发表时间：
2016
影响因子：
3.1
通讯作者：
Dogliotti E
中科院分区：
文献类型：
--
作者：
Narciso L;Parlanti E;Racaniello M;Simonelli V;Cardinale A;Merlo D;Dogliotti E
越来越多的证据表明，控制基因组稳定性的机制对神经系统的发育和功能至关重要。对神经元的主要威胁是DNA氧化损伤，这是通过碱基切除修复（BER）途径修复的。在BER期间产生的参与单链断裂（SSB）加工的酶的功能突变与表现出重要的神经改变和认知能力下降的综合征有因果关系。在这篇综述中，将特别关注与SSB修复相关的神经综合征和与年龄相关的神经退行性疾病的脑区域和神经元选择性，着重讨论神经发生过程中BER的可塑性以及高效BER对正确脑功能的重要性。
There is a growing body of evidence indicating that the mechanisms that control genome stability are of key importance in the development and function of the nervous system. The major threat for neurons is oxidative DNA damage, which is repaired by the base excision repair (BER) pathway. Functional mutations of enzymes that are involved in the processing of single-strand breaks (SSB) that are generated during BER have been causally associated with syndromes that present important neurological alterations and cognitive decline. In this review, the plasticity of BER during neurogenesis and the importance of an efficient BER for correct brain function will be specifically addressed paying particular attention to the brain region and neuron-selectivity in SSB repair-associated neurological syndromes and age-related neurodegenerative diseases.