Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases

作     者：Sina Shadfar Sonam Parakh Md Shafi Jamali Julie D.Atkin 

作者机构：Centre for Motor Neuron Disease ResearchMacquarie Medical SchoolMacquarie UniversitySydneyNSW 2109Australia La Trobe Institute for Molecular ScienceLa Trobe UniversityBundooraMelbourneVIC 3086Australia 

出 版 物：《Translational Neurodegeneration》 (转化神经变性病（英文）)

年 卷 期：2023年第12卷第1期

页      面：604-637页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by an Australian National Health and Medical Research Council(NHMRC)Dementia Teams Research Grant(1095215) Macquarie University MQCRF fellowship,Fight MND Foundation,and Motor Neuron Disease Research Australia 

主　　题：Redox dysregulation DNA damage Neurodegeneration Reactive oxygen species Oxidative stress 

摘      要：Redox homeostasis refers to the balance between the production of reactive oxygen species(ROS)as well as reactive nitrogen species(RNS),and their elimination by *** is linked to all important cellular activities and oxidative stress is a result of imbalance between pro-oxidants and antioxidant *** stress perturbs many cellular activities,including processes that maintain the integrity of *** acids are highly reactive and therefore particularly susceptible to *** DNA damage response detects and repairs these DNA *** DNA repair processes are therefore essential for maintaining cellular viability,but they decline considerably during *** damage and deficiencies in DNA repair are increasingly described in age-related neurodegenerative diseases,such as Alzheimer’s disease,Parkinson’s disease,amyotrophic lateral sclerosis and Huntington’s ***,oxidative stress has long been associated with these ***,both redox dysregulation and DNA damage increase significantly during aging,which is the biggest risk factor for neurodegenerative ***,the links between redox dysfunction and DNA damage,and their joint contributions to pathophysiology in these conditions,are only just *** review will discuss these associations and address the increasing evidence for redox dysregulation as an important and major source of DNA damage in neurodegenerative *** these connections may facilitate a better understanding of disease mechanisms,and ultimately lead to the design of better therapeutic strategies based on preventing both redox dysregulation and DNA damage.