Figure 9. BM-MSC-EVs-carried miR-29c-3p inhibits BACE1 in AD. BM-MSC-EVs could be internalized by neuronal cells and then released their carried miR-29c-3p to upregulate miR-29c-3p expression in neurons. The upregulation of miR-29c-3p inhibited BACE1 and then activated the Wnt/β-catenin pathway to reduce levels of Aβ1-42 and inflammatory cytokine (IL-1β, IL-6 and TNF-α), thereby playing a therapeutic role in the treatment of AD.