This is consistent with previous studies showing that NF-α1/CPE overexpression in 3xTg-AD mice can down regulate the expression of APP transcriptionally and translationally, and reduce the production of insoluble Aβ1-42 in the hippocampus 22 Moreover, the positive relationship and the ability of NF-α1/CPE to prevent and reverse spatial memory deficits, normalize hippocampal synaptogenesis and microglial cell anomalies in pre- 22 and post-symptomatic mice reported here for different AD mouse models, emphasizes its potential in preventing and treatment of AD. This evidence concerns the gene CPE and Alzheimer disease.