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:: Volume 3, Issue 1 (Winter - 2015) ::
Shefaye Khatam 2015, 3(1): 145-156 Back to browse issues page
Alzheimer’s Disease: The Effect of Nrf2 Signaling Pathway on Cell Death Caused by Oxidative Stress
Shahnaz Babaei Abraki, Sara Chavoshi-Nezhad *
Departments of Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran. , sara.chavoshinezhad@gmail.com
Abstract:   (4524 Views)

Introduction: There is an increasing prevalence of Alzheimer's disease (AD). Amyloid-beta deposition and neurotoxicity play an effective role in AD. Oxidative stress is thought to be central in the pathogenesis that leads to production of reactive oxygen species and causing damages of the macromolecules in target cells. It has been reported that the nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of endogenous inducible defense systems in the body and increase the level of many antioxidants, including glutathione-s-transferase. Under oxidative damage conditions, Nrf2 translocates to the nucleus, binds to the antioxidant response element (ARE), and enhances sequence to initiate transcription of cytoprotective genes. This review focuses on cellular mechanisms of Nrf2 regulation and discusses the relationship between Nrf2 regulation and AD. Conclusion: In general, we suggest that Nrf2-ARE activation is a novel neuroprotective pathway that can be consider as a promising therapeutic strategy for the treatment of neurodegenerative disorders, such as AD.

Keywords: Alzheimer Disease, Amyloid beta-Peptides, Oxidative Stress, Reactive Oxygen Species
Full-Text [PDF 518 kb]   (3092 Downloads)    
Type of Study: Review --- Open Access, CC-BY-NC | Subject: Molecular Neurobiology



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Babaei Abraki S, Chavoshi-Nezhad S. Alzheimer’s Disease: The Effect of Nrf2 Signaling Pathway on Cell Death Caused by Oxidative Stress . Shefaye Khatam. 2015; 3 (1) :145-156
URL: http://shefayekhatam.ir/article-1-661-en.html


Volume 3, Issue 1 (Winter - 2015) Back to browse issues page
مجله علوم اعصاب شفای خاتم The Neuroscience Journal of Shefaye Khatam
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