Previous studies performed in animals subjected to scopolamine model of dementia, which mimics the memory deficit observed in diseases characterized by impairment in cholinergic neurotransmission, such as AD [146–148], have shown a marked reduction in the ATP levels and changes in ectonucleotidase activities (E-NTPDase, E-5′-nucleotidase, and ADA), in the cerebral cortex and hippocampus of rats [149, 150]. The gene discussed is ADA; the disease is Alzheimer disease.