Our results have shown that there is no change in the expression levels of the APP, PS-1, and the key APP processing molecules between anti-ERMAP and control Ab-treated AD mice, suggesting that the reduced Aβ plaque load in anti-ERMAP mAb-treated AD mice is not due to decreased APP production and/or processing, but rather likely mediated via increased Aβ clearance. This evidence concerns the gene ERMAP and Alzheimer disease.