After ischemia, neurons of TgM83+/− mice accumulated cytosolic, dendritic, and perinuclear deposits of pathologic α-synuclein as has been reported for TgM83+/− mice challenged with synthetic α-synuclein fibrils or brain homogenates of patients with multiple system atrophy (MSA) [10, 29, 32, 57]. This evidence concerns the gene SNCA and multiple system atrophy.