Overexpression of MEG3 has been shown to reduce Aβ 25–35 deposition and the oxidative stress along with reduction of inflammatory signals through downregulation of IL1β, IL6, and TNFα as well as inhibition of Phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt) signaling cascades in the hippocampus tissues of AD rat models [124]. This evidence concerns the gene MEG3 and Alzheimer disease.