Since SST and CCK cells decline in the APPNL−F/NL−F knock-in mouse model of AD (Shi et al., 2019), this distribution could be due to a subgroup of SST interneurons compensating for the reduction in numbers by upregulating α5 GABAAR expression, interestingly, some studies show upregulated α5 subunits in SP and oriens of the CA1 region (Kwakowsky et al., 2018). This evidence concerns the gene IGKV2D-26 and Alzheimer disease.