Interestingly, the mutation-independent formation of the conformational variant of the p53 protein was AD-specific, as in vitro models (human embryonic kidney [HEK] and differentiated neuroblastoma SHSY5Y cells) overexpressing the APP751 protein and exposure of fibroblasts from non-AD subjects to nanomolar Aβ1–40 and Aβ1–42 concentrations induced the conformational change in the p53 protein (Fig. 3) [56–58]. The gene discussed is TP53; the disease is neuroblastoma.