These include the buildup of disease-specific misfolded proteins (Aβ peptides and tau in AD, α-synuclein in PD, TDP-43 in ALS, mutant huntingtin (mHTT) in HD), ongoing neuroinflammation, oxidative stress, mitochondrial dysfunction, and progressive neuronal loss [7], [8], [9], [10], [11], [12], [13], [14]. This evidence concerns the gene TARDBP and Huntington disease.