期刊
CELLS
卷 10, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/cells10081884
关键词
NF-kappa B; neurodegeneration; oxidative stress; reactive oxygen species; inflammation
类别
资金
- Research Manitoba Fellowship [1913]
- St. Boniface Hospital Research Foundation [1406-3216, 1410-3216]
- Canadian Institute of Health Research (CIHR) [PJT-162144]
- Alzheimer's Society of Manitoba
- Honourable Douglas and Patricia Everett, Royal Canadian Properties Limited Endowment Fund [1403-3131]
- Research Affiliate of the Centre on Aging
- Alzheimer's Soc. of Manitoba and Research Manitoba
Nrf2 impairments in neurodegenerative disorders, such as Alzheimer's disease, lead to oxidative stress, while Nrf2 activators can reverse memory and synaptic plasticity impairments associated with AD.
Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important transcription factor that reduces oxidative stress. When reactive oxygen species (ROS) or reactive nitrogen species (RNS) are detected, Nrf2 translocates from the cytoplasm into the nucleus and binds to the antioxidant response element (ARE), which regulates the expression of antioxidant and anti-inflammatory genes. Nrf2 impairments are observed in the majority of neurodegenerative disorders, including Alzheimer's disease (AD). The classic hallmarks of AD include beta-amyloid (A beta) plaques, and neurofibrillary tangles (NFTs). Oxidative stress is observed early in AD and is a novel therapeutic target for the treatment of AD. The nuclear translocation of Nrf2 is impaired in AD compared to controls. Increased oxidative stress is associated with impaired memory and synaptic plasticity. The administration of Nrf2 activators reverses memory and synaptic plasticity impairments in rodent models of AD. Therefore, Nrf2 activators are a potential novel therapeutic for neurodegenerative disorders including AD.
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