For instance, in murine brain microglial cells, several pro-inflammatory mediators such as LPS, TNFα, CD40/CD40 ligand, and other TLR agonists, up-regulate the expression of Fpr2, which mediates the chemotactic response of the cells to amyloid 1–42 (Aβ42), a pathogenic factor in Alzheimer's disease (AD). This evidence concerns the gene CD40LG and Alzheimer disease.