SOD1 and amyotrophic lateral sclerosis: Importantly, some of these actions effectively translated from normal and SOD1 (G37R) mutation neuronal cultures into a well-characterized SOD1 (G93A) mouse model of ALS to provide improved glucose tolerance, a preservation of lumbar spinal cord structure and neuron density, an amelioration of the loss of specific spinal cord markers, a concomitant reduction in apoptotic markers in spinal cord, and a change in wheel running behavior towards that of the wild-type.