The clearance of beta-amyloid is impaired by several factors, with emphasis on the genetic predisposition of AD patients, who may eventually carry the apolipoprotein E4 (ApoE4), PICALM, and APOJ genes, in addition to presenilin polymorphisms (PSEN1 and PSEN2), which are subunits of γ-secretase.(22,46,47) Despite their neuroinflammatory actions, there is not enough scientific evidence to demonstrate a direct causal relation between the presence of beta-amyloid oligomers and AD, although these can trigger neurodegenerative and toxic conditions characteristic of the disease. This evidence concerns the gene APOE and Alzheimer disease.