ABSTRACT
Chronic inflammation mediated by microglial cells is the fundamental process contributing to the death of dopamine (DA)-producing neurons in the brain. Production of inflammatory products by these microglial cells characterizes the slow destructive process in Parkinson's disease (PD). The activation of microglial cells and the generation of pro-inflammatory cytokines that characterize PD are mediated by several different signaling pathways, with the activation of the respiratory burst by microglial cells being a critical event in the ultimate toxicity of DA-neurons. The work on our lab is concerned with understanding the mechanisms of activation, response, and therapeutic targets of microglial cells, with the aim to provide more effective treatments for PD and other inflammatory diseases of the CNS.
