Both viruses can directly infiltrate the BBB via infected macrophages by stimulating the release of tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) leading to the activation of M1 pro‐inflammatory microglia phenotype resulting in the AD pathological hallmarks deposition in the brain on the long term.22 This evidence concerns the gene TNF and Alzheimer disease.