BDNF mRNA was reduced in the cerebellum of Atxn1154Q/2Q mice (a mouse model of SCA1) at the early symptomatic stage, and the pharmacological delivery of recombinant BDNF into the lateral ventricle during the early disease stage improved the rotarod performance and ameliorated the PC pathology, as was seen from the larger molecular layer thickness and normal calbindin intensity in the treated Atxn1154Q/2Q mice [7]. The gene discussed is CALB1; the disease is spinocerebellar ataxia type 1.