Many decades of clinicopathologic investigations on sporadic Alzheimer's disease (AD) have enormously contributed to the definition of the main pathologic lesions associated with AD, i.e. β-amyloid neuritic plaques (Aβ-NP) and tau-neurofibrillary tangles (tau-NFT), and to a better understanding of the possible relationships between cognitive deficits and AD lesions [1, 2]. This evidence concerns the gene MAPT and Cognitive impairment.