Spinocerebellar ataxia (SCA) is a group of autosomal dominant neurodegenerative diseases, which is characterized by the progressive motor dysfunction and cerebellar atrophy. SCA is classified into SCA1-49 by the differences in the loci of causal genes. Although common functions of SCA causal proteins have not been identified, I assume that there are molecular mechanisms commonly for various SCAs. Therefore, we attempted to identify the common molecular mechanism for SCA. We have already reported that chaperone-mediated autophagy (CMA), one of the proteolytic pathways, is impaired in cell models of SCA14 and SCA21 using our original method to assess CMA activity in a single cell. We further revealed that several other SCA causing proteins also impair CMA activity in AD293 cells. Next, we evaluated the effect of SCA-causing proteins on the morphology of primary cultured Purkinje cells (PCs). To express 7 different SCA-causing proteins in primary cultured PCs, we utilized adeno-associated viral serotype 9 (AAV9) vectors. PC. SCA-causing proteins commonly induced the shrinkage of PC dendrites. We have recently demonstrated that D-cysteine alleviated the dendritic shrinkage in PCs expressing SCA-causing proteins via the activation of CMA. Therefore, CMA would be a novel therapeutic target commonly for various types of SCA.