The amyloid cascade hypothesis still dominates the etiology of AD, which reveals the temporal characteristics of AD brain pathological changes: that β-amyloid (Aβ) deposition occurs early, followed by changes in brain function and metabolism, and alterations in biomarkers of neurodegeneration, such as tau-mediated neuronal injury and structural changes, eventually lead to cognitive impairment (Mattsson et al., 2009; Jack et al., 2010; García-Ribas et al., 2014). The gene discussed is MAPT; the disease is Alzheimer disease.