Moreover, recent findings in cultured neurons from triple-transgenic AD mice, the 3xTg-AD, overexpressing mutant amyloid precursor protein (APP), presenilin 1 (PS1), and h-tau indicate that the pro-AD environment fostered by these mutants enhances ROS generation and ROS-mediated [Zn2+]i mobilization from intracellular Zn2+- binding proteins, thereby providing a potential mechanism for the initiation of the intraneuronal aggregation of Aβ [11], [12]. This evidence concerns the gene APP and Alzheimer disease.