APP and Alzheimer disease: Aβ is an end product of amyloid precursor protein (APP) through amyloidogenic processing cleaved by β‐ and γ‐secretase.1, 2 Emerging documentations show that the secretion of Aβ‐degrading enzymes such as insulin‐degrading enzyme and neprilysin are decreased with ageing, and this could disturb the homeostasis of Aβ and causes Aβ deposition and amyloid plaque formation, ultimately leading to neuronal cell death.3, 4 Symptomatic treatments which include cholinesterase inhibitors and N‐methyl‐D‐aspartate receptor non‐competitive antagonists are currently available to diminish AD symptoms.