Aβ interaction with ApoE-particles is potentiated by sulfatedderivatives of galactocerebrosides, the concentration of which in the brain is lower in AD[2, 46, 47].An agonist of the nuclear retinoid X receptor rapidly increases the production of ApoE andpromotes Aβ degradation, decreasing the formation of Aβ-plaques[48]. Here, APOE is linked to Alzheimer disease.