At these predefined endpoints, none of the animals displayed any overt signs of neurological illness, such as kyphosis, ataxia, or loss in body weight, which TgM83+/− mice develop given enough time after challenge with preformed fibrils of α-synuclein or brain homogenates of patients with multiple system atrophy containing α-synuclein aggregates [10, 32, 57]. This evidence concerns the gene SNCA and cerebellar ataxia.