To investigate whether IGF-1R hyperactivation, as caused by altered longevity-assurance activity of p53:p44, could cause AD-like neurodegeneration in vivo, we bred homozygous p44-transgenic mice (p44+/+) with heterozygous APP695/swe mice, which express a modified mouse APP cDNA encoding the 695-amino acid isoform with a ‘humanized’ amyloid β-peptide (Aβ) domain that includes the familial AD-associated Swedish double mutation (K595N/M596L). This evidence concerns the gene TP53 and Alzheimer disease.