MBP and multiple system atrophy: Since MSA is histologically characterized by αS-immunoreactive cytoplasmic inclusions in oligodendrocytes [2], the pathogenic mechanism of MSA may be attributable to alteration of oligodendrocytes by accumulation of αS. In this context, tg MSA mouse models have been established with expression of full-length wild-type or disease-linked mutant αS under control of oligodendroglia-specific promoters such as 2′,3′-cyclic nucleotide 3′-phosphodiesterase [52], myelin basic protein [53], and proteolipid protein [54].