AD pathogenesis has also been related with novel biomarkers as p53 protein, since Lanni et al. [34] observed in 2007 that unfolded p53 peptide is highly expressed in fibroblast of non-AD patients in the presence of nanomolar concentrations of Aβ peptide, suggesting that the presence of low and non-toxic levels of this biomarker could induce cell changes, including the formation of an abnormal tertiary conformation of p53 which must appear before the start of amyloidogenic cascade. The gene discussed is TP53; the disease is Alzheimer disease.