In prior studies we showed that treatment with Aβ 12-28 P, a peptide homologous to the specific apoE binding domain of Aβ in two AD Tg mouse models with primarily amyloid plaque deposition and in one AD model with primarily CAA resulted in a significant reduction of Aβ burden in both brain parenchyma and in brain vessels compared to age matched vehicle-treated Tg mice16–18. This evidence concerns the gene APOE and Alzheimer disease.