These mutations often cause the formation of protein aggregates such as tau in AD (Matsuo et al., 1994; Castellani, 2020), alpha-synuclein in PD (Spillantini et al., 1997), Huntingtin (Arrasate and Finkbeiner, 2012), and TDP-43 in ALS (Neumann et al., 2006) and may influence vesicular biogenesis, trafficking and affect synaptic transmission (Table 1). This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.