GAD1 and Alzheimer disease: The LEC was unique in this change, since we report unchanged PV cell densities in other cortical regions, including the dorsal entorhinal cortex, neocortex and hippocampus in late phenotypical expression of AD in AppNL-F/NL-F mice, although a general loss of colocalized PV with GAD67 was consistent in all cortical regions studied, suggesting a reduction of the synthesis of GABA neurotransmitter present within cell bodies and therefore inhibitory function.