Amyotrophic lateral sclerosis (ALS), which clinically manifests by progressive muscle atrophy and paralysis, is a fatal neurodegenerative disease characterized by the death of upper and lower motor neurons (MN; Boillee et al, 2006). Individuals with ALS most commonly die of respiratory failure or pneumonia within 3–5 years from initial diagnosis (Pisa et al, 2016). Currently, the glutamate release inhibitor, riluzole, and recently approved free radical scavenger, edaravone, are the only medications approved by the FDA for ALS, and therefore, there remains a strong need for new treatment strategies (Lacomblez et al, 1996; Faes & Callewaert, 2011; Ittner et al, 2015; Hardiman & van den Berg, 2017). Furthermore, eligibility for edaravone was restricted to patients with a relatively short disease duration and preserved vital capacity, indicating a need for a more encompassing treatment (Hardiman & van den Berg, 2017; Maragakis, 2017; Sawada, 2017). For most patients, the underlying cause for ALS is not known (sporadic ALS), but over 100 different mutations in superoxide dismutase 1 (SOD1) account for < 20% of familial ALS forms (Cozzolino & Carri, 2012). Transactive response (TAR) DNA‐binding protein 43 (TDP‐43) and fused in sarcoma (FUS) have also been genetically and pathologically linked to ALS; however, the underlying mechanisms by which these induce ALS pathology and the causal relationship between these events and the death of the motor neurons remain unclear (Mackenzie et al, 2010).