Noted examples include ɑ-Synuclein Lewy bodies in Parkinson’s disease, Tau neurofibrillary tangles in Alzheimer’s disease, Superoxide dismutase 1 (SOD1)-mediated aggregates in Amyotrophic Lateral Sclerosis, and mutant Huntingtin protein aggregates in Huntington’s disease [24–28]. This evidence concerns the gene SOD1 and juvenile Huntington disease.