Importantly, it has been demonstrated that targeted overexpression of ACE in CD115+ myelomonocytic cells (i.e., monocytes, macrophages, microglia) in the double-transgenic APPSWE/PS1ΔE9 murine models of AD (AD+ mice), increased cerebral Aβ clearance, curbed neuroinflammation, and strikingly, preserved memory and learning functions (Bernstein et al., 2014). Here, ACE is linked to Alzheimer disease.