Many of these pathologies are produced by deposits of proteins as Huntingtin in the case of Huntington disease (HD), α-synuclein for Lewy body in Parkinson’s disease (PD), neurofibrillary tangles by hyperphosphorylation of tau (τ) protein, and senile plaques by accumulation of β-amyloid (Aβ) peptide in Alzheimer’s disease (AD) (Myers, 2004; Paulsen, 2011; Jucker and Walker, 2012; Jucker and Walker, 2013). This evidence concerns the gene HTT and Parkinson disease.