DCTN1 and amyotrophic lateral sclerosis: Although the evidence stated above mainly points towards a gain-of-function mechanism in DCTN1-ALS, multiple studies reported that reducing or ablating the levels of the DCTN1 orthologues in either C.elegans [468], Drosophila [469] or zebrafish [470] results in motor deficits and axonal pathology independent of DCTN1 aggregation.