Novel therapeutic modalities are now aimed at proximal disease mechanisms in degenerative ataxias, for example targeting expression of genes containing disease-related triplet repeat expansions in spinocerebellar ataxias (SCAs)1-3 and alpha-synuclein aggregation in multiple system atrophy (MSA).4 One major barrier to the successful development of therapies that slow or stop progression of movement disorders is a lack of tools that can reliably quantify disease worsening over the duration of a clinical trial. Here, SNCA is linked to multiple system atrophy.