The triple-transgenic model (3×Tg-AD), which harbours APPSWE, presenilin-1 (PS1M146V) mutation, and tau mutation (tauP301L), offers the advantage of developing progressive plaque deposition and tangle formation together with microglial activation and an upregulation of the pro-inflammatory cytokine TNFα and chemokine MCP-1 (CCL2), although this is limited to the entorhinal cortex [9]. The gene discussed is CCL2; the disease is Alzheimer disease.