Thus, although a long-term intracerebroventricular (icv) infusion of Aβ1–42 or pro-oxidative cation Fe2+ + Aβ1–42 in young adult rats was ineffective in triggering the production of AD markers in the brain, a combination with the inhibitor of glutathione (GSH) synthesis led to a memory decline and accompanied neurotoxicity-related changes (neuronal loss, increased level of p-Tau and Aβ accumulation). This evidence concerns the gene MAPT and Alzheimer disease.