Thus, deposition of ApoE-Aβ complexes and BAβACs within Aβ plaques in the AD brain represents the gradual outcome of such molecular interactions as end-point signs of decades of malfunctioning Aβ-effectors complexes such as BAβACs and the related abnormality in acetylcholine homeostasis in the brain. This evidence concerns the gene APOE and Alzheimer disease.