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Role of the K eap1/ N rf2 pathway in neurodegenerative diseases
Author(s) -
Yamazaki Hiromi,
Tanji Kunikazu,
Wakabayashi Koichi,
Matsuura Shin,
Itoh Ken
Publication year - 2015
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12261
Subject(s) - oxidative stress , pathogenesis , autophagy , transcription factor , neurodegeneration , biology , disease , population , microbiology and biotechnology , medicine , immunology , gene , genetics , pathology , biochemistry , apoptosis , environmental health
As the elderly population increases, a growing number of individuals suffer from age‐associated neurodegenerative diseases, such as A lzheimer's disease ( AD ) and P arkinson's disease ( PD ). Oxidative stress is considered to play a crucial role in the pathogenesis of age‐related diseases. The transcription factor N rf2 (nuclear factor erythroid 2‐related factor 2) is activated by oxidative stress and regulates the expression of a variety of antioxidant enzymes and proteins that exert cytoprotective effects against oxidative stress. Numerous studies have addressed the role of N rf2 in age‐related diseases, including neurodegenerative diseases, using animal or in vitro cell culture models. Here, we introduce the role of oxidative stress in the pathogenesis of neurodegenerative diseases and critically examine the recent findings concerning the role for N rf2 in the amelioration of AD and PD . N rf2 not only regulates antioxidant proteins but also regulates the genes associated with autophagy and nerve growth factor signaling. Current research unequivocally demonstrates that the activation of the N rf2 pathway is a promising novel strategy for the prevention and modification of neurodegenerative diseases.