Several studies have reported that the activity of the canonical Wnt/β-catenin pathway and its associated members such as Wnt-2, Wnt-3a, Wnt-7a, Wnt-5a, Fzd1, Fzd2, β-catenin, Cyclin D1 and GSK-3β is largely deregulated in the astrocytes and MNs extracted from the spinal cord of G93A superoxide dismutase-1 (SOD1) transgenic mouse model of ALS [176–179]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.