Moreover dynein and ALS mutant SOD1 appeared to mostly colocalise in ALS mutant SOD1 protein aggregates in cultured motor neurons (Ligon et al., 2005) and in vivo in SOD1G93A and G85R transgenic mice (Zhang and Zhu, 2006) supporting the notion that reduced retrograde axonal transport in SOD1-related ALS may at least in part be caused by sequestration of dynein. Here, SOD1 is linked to amyotrophic lateral sclerosis.