In CSF, a combination of low levels of the 42-aminoacid isoform of amyloid beta (Aβ42) and high levels of total tau (t-Tau) and phosphorylated tau (p-Tau) is thought to reflect the two widely accepted pathophysiological hallmarks of AD: amyloid plaques and neurofibrillary tangles [2]. This evidence concerns the gene MAPT and Alzheimer disease.