Paradoxically, while normal prostate physiology prioritizes polyamine synthesis (e.g., spermine), regulated by androgen-dependent enzymes like ODC to support secretory functions, PCa progression exhibits a contradictory polyamine landscape: spermine levels decline sharply despite ODC overexpression, a phenomenon contrasting with polyamine accumulation patterns in other cancers. This evidence concerns the gene ODC1 and posterior cortical atrophy.