TARDBP and amyotrophic lateral sclerosis: The increased ATP hydrolysis and putative co-chaperone independence possibly contribute to these variants more effectively disaggregating and alleviating toxicity of exogenous human aggregating peptides associated with amyotrophic lateral sclerosis (ALS, i.e., TDP-43 and FUS) and Parkinson’s Disease (i.e., α-synuclein) [39], as well as remodeling aggregates associated with systemic Transthyretin amyloidosis in vivo [40].