To do this, we utilized the SCA1 knock-in (KI) mouse model, which expresses Atxn1 [154Q] under its endogenous regulators, and replicates many key aspects of SCA1 disease progression and pathology, including progressive behavioral and cognitive impairments, as well as mutant ataxin-1 aggregation, gliosis, and PC pathology [10]. This evidence concerns the gene ATXN1 and Cognitive impairment.