Abnormalities in ASM bioactivity result in disturbed sphingomyelin degradation and ceramide generation, leading to extreme accumulation of sphingomyelin but deficient ceramide production.1, 13 Aberrant ASM-dominated sphingomyelin-ceramide signaling is associated with numbers of human nervous disorders including Alzheimer disease, Parkinson disease, schizophrenia,and depression.13 In particular, ASM deficiency contributes to lipid storage disorders, i.e., Niemann–Pick disease.11, 14. This evidence concerns the gene SMPD1 and early-onset autosomal dominant Alzheimer disease.