Our data from human samples, while correlational, suggest that a loss of nuclear TDP-43 in capillary ECs may alter the cellular response to nuclear p65/NF-κB levels, and could also be linked to changes in Wnt/β-catenin signaling; however, isolating alterations in TDP-43 from the other changes in AD, ALS and FTD is challenging, making causal attribution unclear. The gene discussed is NFKB1; the disease is amyotrophic lateral sclerosis.