文献类型：期刊文献

英文题名：Nrf2: a dark horse in Alzheimer's disease treatment

作者：Osama, Alsiddig[1,2];Zhang, Junmin[1,2,3];Yao, Juan[4];Yao, Xiaojun[1,2,3];Fang, Jianguo[1,2]

第一作者：Osama, Alsiddig

通信作者：Yao, XJ[1];Fang, JG[1];Yao, XJ[2];Fang, JG[2];Yao, XJ[3]

机构：[1]Lanzhou Univ, State Key Lab Appl Organ Chem, Lanzhou 730000, Peoples R China;[2]Lanzhou Univ, Coll Chem & Chem Engn, Lanzhou 730000, Peoples R China;[3]Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Ave Wai Long, Taipa, Macau, Peoples R China;[4]Gansu Univ Chinese Med, Sch Pharm, Lanzhou 730000, Peoples R China

第一机构：Lanzhou Univ, State Key Lab Appl Organ Chem, Lanzhou 730000, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, State Key Lab Appl Organ Chem, Lanzhou 730000, Peoples R China;[2]corresponding author), Lanzhou Univ, Coll Chem & Chem Engn, Lanzhou 730000, Peoples R China;[3]corresponding author), Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Ave Wai Long, Taipa, Macau, Peoples R China.

年份：2020

卷号：64

外文期刊名：AGEING RESEARCH REVIEWS

收录：;Scopus(收录号：2-s2.0-85095435841);WOS:【SCI-EXPANDED(收录号:WOS:000595936000009)】；

基金：Financial supports from the National Natural Science Foundation of China (21778028 & 22077055), the Natural Science Foundation of Gansu Province (20JR5RA311 & 18JR4RA003) and the 111 project are greatly acknowledged. The author (Alsiddig Osama) is grateful to the Chinese Scholarship Council for funding his study program, and Junmin Zhang is grateful to Macao Young Scholars Program (AM201926).

语种：英文

外文关键词：Alzheimer's disease; Nrf2; Keap1; Amyloid beta-peptide; Tau protein; Oxidative Stress

摘要：Alzheimer's disease (AD), an age-dependent neurodegenerative disorder, is the main cause of dementia. Common hallmarks of AD include the amyloid beta-peptide (A beta) aggregation, high levels of hyperphosphorylated tau protein (p-tau) and failure in redox homeostasis. To date, all proposed drugs affecting A beta and/or p-tau have been failed in clinical trials. A decline in the expression of the transcription factor Nrf2 (nuclear factor-erythroid 2-p45 derived factor 2) and its driven genes (NQO1, HO-1, and GCLC), and alteration of the Nrf2-related pathways have been observed in AD brains. Nrf2 plays a critical role in maintaining cellular redox homeostasis and regulating inflammation response. Nrf2 activation also provides cytoprotection against increasing pathologies including neurodegenerative diseases. These lines of evidence imply that Nrf2 activation may be a novel AD treatment option. Interestingly, recent studies have also demonstrated that Nrf2 interferes with several key pathogenic processes in AD including A beta and p-tau pathways. The current review aims to provide insights into the role of Nrf2 in AD. Also, we discuss the progress and challenges regarding the Nrf2 activators for AD treatment.