It is widely believed that inhibition of ALP function contributes to the aberrant accumulation of protein species in age-related neurodegenerative disease that not only define disease-specific neuropathology but also may contribute to disease pathogenesis, including alpha synuclein (α-syn) in Parkinson's disease and metabolites of amyloid precursor protein (APP) in Alzheimer's disease [12]–[15]. This evidence concerns the gene APP and Alzheimer disease.