The function of ataxin-2 is unknown but expansion of the polyglutamine (polyQ) tract from normally 22 to ≥32 repeats causes a late-onset, autosomal dominant ataxia (spinocerebellar ataxia type 2, SCA2), levodopa-responsive Parkinsonism and various cognitive deficits involving mainly executive function and verbal memory [1]–[4]. This evidence concerns the gene ATXN2 and spinocerebellar ataxia type 2.