MicroRNA-34a was found to target ADAM10 expression, leading to reduced ADAM10 protein in various brain regions and increased intraneuronal Aβ accumulation.82 Likewise, also age-related increases in miR-138 in APP/PS1 mice lowered ADAM10 expression, leading to higher Aβ production and resulting in synaptic and cognitive deficits, while its suppression reversed these effects.83 Together, these data suggest that increased microRNA activity suppresses ADAM10 expression, inactivating the non-amyloidogenic pathway and resulting in elevated Aβ production (Figure 3, Table 2). Here, ADAM10 is linked to Cognitive impairment.