In conclusion, in the present study GA was demonstrated to have compound-specific effects useful to prevent Aβ accumulation in the mouse brain, being capable at the same time of 1) interfering with Aβ polymerization, 2) stimulating the ApoE and MDR1 detoxification system of mouse cortical astrocytes and the brain tissue, and 3) reducing Aβ deposition in the brain of TgCRND8 mice, an animal model of AD. This evidence concerns the gene APOE and Alzheimer disease.