This may be a compensatory mechanism for trafficking deficits of cargoes to the lysosomal compartment, or an attempt to compensate for deficits in the production of the active form of Cathepsin D. In summary, our results illustrate that Purkinje cells in SCA6 mice have an impaired ability to degrade other endocytosed cargo beyond BDNF and TrkB. The gene discussed is CTSD; the disease is spinocerebellar ataxia type 6.