In favor of this hypothesis are also in vivo studies on AD mouse animal models, showing that cognitive deficit is prevented by apoA-I overexpression (Lewis et al., 2010), while it is worsened by its deletion (Lefterov et al., 2010), and i.v., administration of HDL reduces soluble Aβ brain levels (Robert et al., 2016). Here, APOA1 is linked to Alzheimer disease.