APP and Alzheimer disease: Pathologically, senile plaques, including amyloid beta (Aβ) and carboxy-terminal fragments (CTFs) are derived via amyloid precursor protein (APP) proteolysis, and neurofibrillary tangles, including hyperphosphorylated tau, are two representative hallmarks of AD.1, 2, 3 Together with the accumulation of Aβ, local inflammation, altered hippocampal neurogenesis and synaptic loss have been correlated with cognitive deficits in AD patients.4, 5 However, no treatment has yet been developed that can cure or prevent the progression of dementia.