The pathogenic cleavage processing of amyloid precursor protein (APP) is thought to be one of the starting blocks leading ultimately to these hallmark characteristics of AD and involves increased β-secretase cleavage leading to the production of beta amyloid (Aβ) fragments 40 and 42 (Aβ40, Aβ42) and intracellular C-terminal fragments (βCTFs) [2]. This evidence concerns the gene APP and Alzheimer disease.