MBP and multiple system atrophy: Oligodendroglial dysfunction may also be a primary event in MSA pathogenesis 82, but it is plausible that the accumulation of α‐synuclein in oligodendrocytes may deepen and broaden this dysfunction resulting in reduced trophic support and demyelination, as suggested by findings in the MBP‐α‐synuclein transgenic mouse model of MSA 66, 92.