Accumulation of Aβ together with hyper-phosphorylation of the microtubule-associated protein Tau are hypothesized to underlie reduced synaptic transmission, neuronal dysfunction and neurodegeneration in AD (Alonso et al., 1996; reviewed in Hardy and Selkoe, 2002; Zussy et al., 2013), though the etiology of the ~95% of “sporadic” late-onset cases is unclear. This evidence concerns the gene MAPT and Alzheimer disease.