In particular, the bradykinetic syndrome can be explained by the presence of CRMP5 in the basal ganglia, ataxia by the presence of GAD65 and CRMP5 in the cerebellum, apathy and executive difficulties by the expression of CRMP5 in the cingulate cortex and frontal regions, and cognitive decline by injuries to all the above-mentioned structures. This evidence concerns the gene DPYSL5 and cerebellar ataxia.