Abstract Title: Neuroinflammation as a therapeutic avenue for Alzheimer's disease treatment The role of neuroinflammation in neurological disorders remains controversial. While triggered by the toxic accumulation of Aβ, Alzheimer's disease (AD) is thought to be potentiated by blood-brain barrier (BBB) breakdown and immune cell infiltration to the brain. However, drugs that inhibit immune cell infiltration to the CNS have failed as treatments for AD. In other disease models, like infection with the neurotropic parasite Toxoplasma gondii, neuroinflammation is required for survival of both mice and humans, yet almost all of the infected population (over 2 billion people worldwide) harbors a life-long asymptomatic infection. Thus, T. gondii infection models an immune response that is robust to control the parasite yet tightly controlled prevent immune mediated pathology in the brain. Our lab has discovered that of the three canonical T. gondii strains, infection with type II parasites protects against Aβ deposition in the brain. Though prolonged inflammation has been shown to promote alternative activation in monocyte lineage cell types, data generated in our lab shows that type II parasites induce a larger population of alternatively activated macrophages in the brain. Therefore, I hypothesize that infection with type II parasites generates a population of phagocytic, alternatively activated macrophages that can more easily access the brain and clear β-amyloid plaques. To test this hypothesis, I will determine the impact type II infection has on the BBB, Aβ clearance from the brain and the populations of immune cells that infiltrate the CNS compared to infection with type III parasites. This strategy will allow me to quickly separate changes in the brain that aid specifically in Aβ clearance from changes that occur during infection in general. Identifying the cell types that are capable of eliminating pathogenic plaques from the brain would lead to new strategies to combat the toxic accumulation Aβ.