TTBK1 and spinocerebellar ataxia type 11: In this study, we have shown that in vivo central administration of ASO-Ttbk1 selectively downregulates Ttbk1 expression in the temporal cortex tissue in PS19 mice without affecting Ttbk2. The catalytic domain of Ttbk2 is highly homologous to Ttbk1 and loss of function mutations of human TTBK2 is genetically linked to spinocerebellar ataxia type 11 [26].