As expected, clustered formations became random closer to amyloid plaques in both Nr3c1+/+-APP/PS1 and Nr3c1ki/ki-APP/PS1 genotypes (P < 0.05, Fig. 3e); clustered eliminations were random in the proximal and intermediate zones except for Nr3c1ki/ki-APP/PS1 mice (P = 0.04). This evidence concerns the gene APP and amyloidosis.