The localization of glutamate decarboxylase (GAD) isoforms to the neocortex, hippocampus, basal ganglia, and cerebellum of AD brains also makes the corresponding change in LT activity with changes in Gln/GABA ratios reasonable as LT GABA production can be expected from GAD activity [62]. The gene discussed is GAD1; the disease is Alzheimer disease.