Although the etiology of AD is still obscure, a mounting body of evidence has demonstrated that extracellular deposition of fibrillar β-amyloid (Aβ) peptide and the aggregation of neurofibrillary tangles containing hyper-phosphorylated tau are the main pathological hallmarks of AD (Yankner et al., 1990; Zlokovic, 2005). The gene discussed is MAPT; the disease is Alzheimer disease.