On the contrary, the evidence that the diminution of GTP-bound membrane active form of Rab5 we contextually detected in the hippocampus does not respond to antibody treatment in immunized AD mice hints at the involvement of other adaptors proteins of the endocytic pathway controlling the APP/BACE1 trafficking (i.e., SorLA) into neurons [162,163] in 12A12-mediated beneficial effects on cerebral Aβ accumulation. Here, RAB5A is linked to Alzheimer disease.