PPIB and Alzheimer disease: For example, in vitro studies have supported that ACE degrades amyloid-β plaques, a pathologic hallmark of AD.5 Animal AD models with heterozygous deletion of the ACE gene demonstrated that a decrease in ACE levels promoted amyloid-β deposition and increased the number of apoptotic neurons.4 At present, there is, therefore, uncertainty surrounding the role of ACE inhibitors in the pathogenesis of AD.