In line, by enhancing oxidative modifications of alpha-synuclein using the mitochondrial inhibitor 3-nitropropionic acid (3NP), neuropathology and neurological deficits exacerbated in both the PLP- and the MBP-driven transgenic MSA model implying increased susceptibility of alpha-synuclein-bearing OLGs toward oxidative stress [187, 197]. The gene discussed is MBP; the disease is multiple system atrophy.