Although the formation and development of SPs and NFTs are two defining characteristics of neuropathological processes in AD, a debate still persists over whether SPs or NFTs play key and causal roles in the neuropathological mechanisms of AD [10]–[13], and a proposal has been raised that the formation of Aβ plaques and hyperphosphorylated Tau may be the consequences of axonopathy [9], [15], [20]. This evidence concerns the gene MAPT and Alzheimer disease.