The most widely accepted theory for the onset of sporadic AD is the accumulation of extracellular Aβ42 in an aggregated state in the brain, subsequently leading to the formation of neurofibrillary tangles (NFT) containing hyperphosphorylated tau proteins and consequently to its inactivation, thus leading to inhibition of binding to the spindle apparatus and hence disrupted axonal transport [9,10]. This evidence concerns the gene MAPT and Alzheimer disease.