TARDBP and amyotrophic lateral sclerosis: Additionally, other ALS-Tdp-43 models with mutations in the C-terminal prion-like domain of murine Tdp-43 sequence [29, 30], likely involves altered spliceosomal complex formation capacity of endogenous Tdp-43 and associated alternative splicing of target mRNA transcripts rather than Tdp-43 aggregation-induced changes in gene expression patterns.