In terms of molecular function, excessive increases in the activating nuclear factor kappa B (NF-kB) have been shown to play an important role in driving Abeta deposition, neuroinflammation and neurodegenerative disease in AD, but NF-kB levels are not increased in PD, which may indicate that NF-kB does not promote α-synuclein (a-SYN) deposition (Lindsay et al., 2021). This evidence concerns the gene NFKB1 and Alzheimer disease.