AD is characterized by the presence of two major pathophysiological hallmarks—formation of extracellular amyloid β (Aβ) plaques derived from the amyloid precursor protein (APP) [6,7] and intracellular neurofibrillary tangles (NFTs) consisting of abnormally hyperphosphorylated τ-protein filaments [8,9,10]. This evidence concerns the gene TBXT and Alzheimer disease.