Although the exact causal link between neuronal injury and microglial activation in PD remains controversial, one of the earliest reported harmful effects demonstrated to cause demise of dopaminergic neurons was microglial-mediated release of proinflammatory cytokines, including IFN-γ [20] IL-1β, TNF-α, IL-2, and IL-6 [88] with elevated levels of TNF-α receptor R1 (p55), bcl-2, soluble Fas, caspase-1 and caspase-3 in postmortem striatum, SN, and CSF of patients with PD [89, 90]. This evidence concerns the gene CASP1 and Parkinson disease.