Based on the published reports we summarized above, regulating the activity/expression of ADE by short peptide and/or chemical agents could be a promising strategy to treat AD and PD; modulation of the expression and/or activity of NEP, IDE, AEP, and ADAM10 presented the clearance of amyloid deposits and improvement of cognitive deficits in vivo. The gene discussed is LGMN; the disease is amyloidosis.