These stringent criteria limited the number of DEGs used in subsequent analyses, but still allowed the uncovering of several genes previously associated with AD pathologies, such as ABCA1, ABCA2, CALB1, C1R, C1S, GAD1/2, PVALB, REST, SLC32A1, SST, VGF, and VIP15–19 The reduced number of DEGs in FLI and TLI likely explains our failure to detect functional annotations associated with synaptic transmission and immune response in GSEA, as previously reported13. This evidence concerns the gene CALB1 and Alzheimer disease.