CD36 upregulation mediated by intranasal LV-NRF2 treatment mitigates hypoxia-induced progression of Alzheimer's-like pathogenesis

There is extensive evidence that oxidative stress induces cellular dysfunction in the brain and plays a critical role in Alzheimer's disease (AD) pathogenesis. Hypoxia increases factors involved in oxidative stress injury and contributes to the onset and progression of AD. Nuclear factor erythr...

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Veröffentlicht in:	Antioxidants & redox signaling 2014-12, Vol.21 (16), p.2208-2230
Hauptverfasser:	Wang, Chun-Yan, Wang, Zhan-You, Xie, Jing-Wei, Cai, Jian-Hui, Wang, Tao, Xu, Ye, Wang, Xu, An, Li
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - genetics Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - genetics Animals CD36 Antigens - genetics CD36 Antigens - metabolism Disease Models, Animal Disease Progression Exons Genetic Therapy Humans Hypoxia Lentivirus Mice Mice, Transgenic Microglia - enzymology Microglia - metabolism NF-E2-Related Factor 2 - genetics Original Research Communications Oxidative Stress - genetics Up-Regulation
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