Our major findings demonstrate that (1) The Nox2 isoform is involved in 6-OHDA-mediated DA degeneration in SN; (2) inhibition of microglial cells by the treatment with minocycline increases the susceptibility of gp91phox-/- 6-OHDA lesioned mice to develop PD, as evaluated by apomorphine-induced rotational behavior and TH immunolabeling; (3) minocycline treatment leads to NF-κB activation and TNF-α release into the SNpc of gp91phox-/- 6-OHDA lesioned mice. This evidence concerns the gene TH and Parkinson disease.