Improper intracellular and extracellular accumulations of mutated and misfolded neuronal proteins are the most obvious hallmarks of NDDs, such as Aβ and C-terminal fragments (CTFs) of the amyloid precursor (APP) in Alzheimer’s disease (AD), mutant alpha-synuclein in Parkinson’s disease (PD), mutant TAR DNA-binding protein 43 (TDP-43) in amyotrophic lateral sclerosis (ALS), mutant huntingtin protein (mHTT) with expanded polyglutamine in Huntington’s disease (HD), etc. [15,16]. This evidence concerns the gene TARDBP and juvenile Huntington disease.