These diseases typically result from the abnormal aggregation of proteins in the CNS, such as amyloid-β (Aβ) plaques and tubulin-associated unit (Tau) for AD, α-synuclein (α-syn) in neurons for PD, α-syn in oligodendrocytes for MSA, TAR DNA-binding protein 43 (TDP-43) for ALS and a type of FTD, leading to gradual deterioration of neural structure and function [1–4]. This evidence concerns the gene TARDBP and frontotemporal dementia.