TARDBP and amyotrophic lateral sclerosis: Conditional depletion or knockout models of TDP-43 have shown ALS-like clinical phenotypes [42] or cellular dysfunctions, including deficits in DNA repair [43], an alteration of TDP-43-transcriptome resulting in synaptic impairment [44], a loss of splicing repressor function [45], and astrocytic activation [46].