Where all Alzheimer’s Disease drugs have failed, we are building a quantitative model of this system to tease out all the genetic and electronic perturbations of the system, its interactions between the different components at the molecular level. We are finding that quantum fluctuations and kinetics are involved with wild type p53 losing its activity when it aggregates, while p53 mutants with enhanced amyloidogenicity, show accelerated aggregation. We will focus on rescuing p53 wildtype protein and inhibiting gain-of-mutant function P53