AD patients have reduced Aβ42 concentrations in cerebrospinal fluid (CSF) [4] or plasma [5], elevated cortical Aβ plaques [6–8], CSF or plasma phosphorylated Tau (p-Tau) concentrations [9], and cortical tau tangles [10], which eventually result in synaptic loss [11–13], hippocampal atrophy [14], Temporal-metaROI cortical thinning [15], hypometabolism and cognitive decline [4, 9, 16]. This evidence concerns the gene MAPT and hippocampal atrophy.