By binding to the nuclear receptors RAR and RXR, they form complexes that function as ligand-dependent transcriptional regulators that bind to specific RAREs present on the promoter regions of target genes that influence pathophysiological pathways of Alzheimer’s disease, such as SOD-1, SOD-2, ABCA1, PLA2, PLC, PSEN1, PSEN2, BACE1, and MAPT. Pharmacologically, retinoids are unstable compounds that rapidly oxidize due to the presence of conjugated double bonds, explaining the short half-life of ATRA and 13-cis RA. This evidence concerns the gene BACE1 and early-onset autosomal dominant Alzheimer disease.