However, there is a lack of correlation between the neuropathological benefits and the expected clinical improvement, due to several suspected reasons: the efficiency of antibodies is maximum on Aβ oligomers that have not yet aggregated in the form of senile plaques, thus requiring administration in the prodromal/early stages; there are also other factors such as age or ApoE which influence the behavior of Aβ oligomers and the interaction with possible antibodies [113]. The gene discussed is APOE; the disease is Senile plaques.