The main targets in AD therapy include Aβ and tau for removing plaques and tangles, Aβ and immune receptors (e.g., TREM2, CD33) to activate microglia, Aβ and BBB transporters (e.g., TfR1, low-density lipoprotein receptor-related protein 1 [LRP1]) to deliver to the central nervous system (CNS), and novel combinations such as Aβ/Beta-site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1) or tau/Glycogen Synthase Kinase-3 Beta (GSK3β) to decrease Aβ formation or tau phosphorylation [52]. This evidence concerns the gene TREM2 and Alzheimer disease.