Previous studies demonstrated that toxicity of Aβ25–35 in models of neurodegenerative diseases in vitro and in vivo was associated with the enhancement of ROS and NO liberation and oxidative damage [37,38,39,40,41], which up-regulated redox-sensitive transcription factors such as NF-κB, an important factor responsible for oxidative and inflammatory reactions in AD [42]. This evidence concerns the gene NFKB1 and Alzheimer disease.