Recently, it has been shown that Ang-1 accelerated the disease progression by promoting the formation of amyloid plaques and Aβ42, and increasing memory and learning impairment in the APP/PS1 transgenic mouse model [135]; however, it has been suggested that hypoxia might underlie such increases in Ang-1 levels in AD, since this pathological condition induces an increase in the expression of this growth factor [134] (Table 3). This evidence concerns the gene ANGPT1 and Alzheimer disease.