In this context, the ADIS-associated upregulation of pro-survival factors (Fig. 4A), downregulation of p53 (Fig. 2A) and the inability to induce downstream p53 effectors, such as Bax (Fig. 6B) serve to abrogate a cytotoxic response to AD and potentially promote persistence of cells that eventually resist ADIS and comprise androgen-refractory outgrowths. This evidence concerns the gene TP53 and Alzheimer disease.