TARDBP and amyotrophic lateral sclerosis: In addition to TDP43-protein aggregates, different mechanisms have been proposed to drive ALS pathogenesis such as impaired proteostasis, disturbed RNA metabolism, nucleocytoplasmic and cytoskeletal and axon-transports defects, impaired DNA repair, vesicle-transport defects, excitotoxicity, mitochondrial dysfunction, neuroinflammation, astrogliosis and oligodendrocyte dysfunction [8,9,10,11,12,13].