A number of recent studies have shown that NPC disease exhibits some striking parallels with AD pathology including i) the presence of tau-positive neurofibrillary tangles [4], [5], ii) the influence of ε4 isoform APOE in promoting disease pathology [6], [34], and iii) endosomal abnormalities associated with the accumulation of cleaved APP derivatives and/or Aβ peptides in vulnerable neurons [11], [35]. This evidence concerns the gene MAPT and Alzheimer disease.