Involvement of genetic interactions in this process is illustrated by the fact that presenilin 1 (PS1), mutants of which produce a familial AD, binds directly to E-cadherin; PS1 displaces p120 from E-cadherin, stabilizes the binding of β- and γ-catenins to E-cadherin, increases linkage of the cadherin/catenin complex to the cytoskeleton, and stimulates Ca2+- and cadherin-dependent cell–cell aggregation [43]. Here, CDH17 is linked to Alzheimer disease.