Over-expression of miR-195 in synj1−/− neurons failing to exhibit any additive effects on lysosomal enlargement (Fig. S6F) further strengthens the concepts that miR-195 rescues AD-related phenotypes through its target gene, synj1. It should be noted that ApoE4+/− carriers exhibit higher sensitivity to miR-195 manipulations than ApoE4−/− subjects (Figs. 4 and S5; Figs. 5 and S6), possibly due to much lower baseline miR-195 levels. Here, APOE is linked to Alzheimer disease.