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To through light on the mechanisms underlying the stimulation and persistence of glial cell activation in Parkinsonism, weinvestigate the function of IFN-c and TNF-a in experimental models of Parkinson’s disease and analyze their relation with localglial cell activation. It was found that IFN-c and TNF-a remained higher over the years in the serum and CNS of chronicParkinsonian macaques than in untreated animals, accompanied by sustained glial activation (microglia and astroglia) in thesubstantia nigra pars compacta. Importantly, Parkinsonian monkeys showed persistent and increasing levels of IFN-cR signalingin both microglial and astroglial cells. In addition, experiments performed in IFN-c and TNF-a KO mice treated with MPTPrevealed that, even before dopaminergic cell death can be observed, the presence of IFN-c and TNF-a is crucial for microglial andastroglial activation, and, together, they have an important synergistic role. Both cytokines were necessary for the full level ofactivation to be attained in both microglial and astroglial cells. These results demonstrate that IFN-c signaling, together with thecontribution of TNF-a, have a critical and cell-specic role in stimulating and maintaining glial cell activation in Parkinsonism

cell death and disease

IFN-γ signaling, with the synergistic contribution of TNF-α, mediates cell specific microglial and astroglial activation in experimental models of Parkinson's disease