In addition, miR-451a overexpression successfully rescued pathologically increased β-secretase metabolites of APP, including Aβ monomer, oligomers, and β-C-terminal fragment (CTF-β) and its key regulator, beta APP cleaving enzyme 1 (BACE1) in the mPFC of such AD model mice (Figure 4F-I). The gene discussed is APP; the disease is Alzheimer disease.