Additionally, upregulation of pro-inflammatory genes was recorded including MAPK1, TLR2, MYD88, and NF-κB1. Each is known to affect AD pathobiology via T cell activation [40, 41, 57], amyloidogenesis [44], neuroinflammation, and neuronal damage [45, 46]. This evidence concerns the gene NFKB1 and Alzheimer disease.