Angiotensin-converting enzyme (ACE) is another Aβ-degrading agent. Captopril, a blood–brain barrier (BBB) penetrating ACE inhibitor, increases Aβ accumulation (Zou et al., 2007), and ACE overexpression in myelomonocytes reduces Aβ deposition in AD model mice (Bernstein et al., 2014). However, brain ACE deficient mice showed no significant alteration in endogenous Aβ levels (Eckman et al., 2006). In addition, two small studies assessing the clinical use of ACE inhibitors, found that they did not deteriorate dementia in AD and amnestic mild cognitive impairment (MCI) patients (Ohrui et al., 2004; Rozzini et al., 2006). Because of such conflicting findings, contributions of ACE to Aβ degradation in the brain per se remain ambiguous.
