It has also been shown that, in the presence of excess apolipoprotein E (ApoE), Aβ interacts with these enzymes and forms highly stable BuChE/AChE-Aβ-ApoE complexes (BAβAC), strongly associated with AD pathology (Darreh-Shori et al., 2011a,b, 2012). The gene discussed is APOE; the disease is Alzheimer disease.