This issue may be of particular therapeutic relevance in the treatment of AD because pro-inflammatory cytokines, including TNF, have been shown to preferentially attenuate phagocytic activity of microglia induced by fibrillar Aβ amyloid peptides (but not by IgG antibody activation of Fc Receptor) through an E prostanoid receptor-dependent mechanism [46]. Here, TNF is linked to Alzheimer disease.