Recent evidence suggests an important role of inflammation in the pathophysiology of AD as demonstrated by the identification of the pro-inflammatory cytokines IL-1α, IL-1β, IL-6, TNF-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IFN-α in the AD brain produced by neurons or microglia, refs. [6,7,8,9,10] endothelial cells and inflammatory cells recruited from the circulation, and by the blood–brain barrier (BBB) when biochemical or mechanical damage occurs [11,12]. Here, TNF is linked to Alzheimer disease.