As significant increased levels of putrescine have been reported in brain tissue from AD patients,39 similar elevations were also observed in the APP/PS1 mice at 6 months of age,26 suggesting Aβ causes upregulation of polyamine uptake and increased ornithine decarboxylase activity, which leads to increased polyamine synthesis,40, 41 which in turn causes dysfunction of the N‐methyl‐D‐aspartate receptor leading to the neuronal excitotoxicity which occurs in AD.42 This evidence concerns the gene APP and Alzheimer disease.