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Evidence is now overwhelming that inflammation is a central process in the pathogen‐ esis of progressive Parkinson's disease (PD). The hallmark of this neuroinflammation is the activation of microglial cells and the secondary role of adaptive immunity in both the familial and idiopathic forms of PD, leading to the loss of dopamine‐producing cells within the Substantia nigra. This activation is characterized by the oxidative stress response, production of inflammatory mediators, recruitment and activation of immune effector cells which create a toxic environment for dopaminergic neurons, and in forming a continuous cycle of inflammatory responses that result in chronic neuroin‐ flammation and progressive neurodegeneration. This chapter focuses on the different components of the inflammatory response that are involved in Dopamine‐neurodegen‐ eration, the evidence for inflammation in different forms of PD, and the role of inflammation in the various animal models of PD. Finally, we provide current evidence that targeting this inflammation with a number of anti‐inflammatory therapies can be an effective way to halt the progression of chronic neuroinflammation‐induced PD.

Inflammation: Role in Parkinson's Disease and Target for Therapy