Inflammation as a Target for Epilepsy Therapy: The Case of Natalizumab

Inflammation results from a cascade of inflammatory mediators, with concomitant anti-inflammatory molecules, often due to trauma, ischemia, infection, or an immune process. The inflammatory mediators arise from tissue, or blood circulating cells, and can involve nonspecific innate immunity or antigen-specific adaptive immunity.1-3 In the brain, these mechanisms are mediated through microglia, astrocytes, neurons, and endothelial cells, as well as leukocytes entering the parenchyma through disruption of the blood–brain barrier. Cytokines are polypeptide mediators of inflammation that are released by these cells and interact with various cognate receptors, leading to an array of pathophysiologic effects that contribute to inflammation.4 Chemokines are a specific type of cytokine that attracts leukocyte migration into the parenchymal injury. These multiple pathways mediating inflammation provide many targets for anti-inflammatory therapies.

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