The downregulation of CSF SCG1 peptide abundance in ALS patients may be attributed to perturbation of secretory pathways, neuronal loss, synaptic dysfunction, decreased density of SCG1 in the neuropil and intracellular accumulation in SOD1 aggregates (Schrott-Fischer et al, 2009). Here, SOD1 is linked to amyotrophic lateral sclerosis.