Huntington’s disease (HD), an inherited autosomal disease [2], is characterized by ‘intraneuronal nuclear inclusions’ (INNs)] composed of insoluble aggregates of extra-long polyglutamine caused by a gain-of-function mutation in the huntingtin (HTT) gene [3,4] causing expansion of cytosine–adenine–guanine (CAG) repeats at the N-terminus of the protein. This evidence concerns the gene HTT and juvenile Huntington disease.