Chronic T. gondii infection enhances the recruitment of monocytes to the brain. These monocytes have a high capacity for phagocytosing Aβ, which can reduce Aβ plaque load.The infection increases the expression of enzymes involved in the degradation of Aβ, such as insulin-degrading enzyme (IDE) and matrix metalloproteinases (MMPs).T. gondii infection has been shown to reduce amyloid burden in various cortical regions, including the prelimbic cortex, retrosplenial cortex, and visual cortex.The hippocampus also shows reduced Aβ deposition following T. gondii infection. The gene discussed is IDE; the disease is infection.