A study using celastrol in a G93A-superoxide dismutase 1 (SOD1) transgenic mouse model of ALS found that orally administrated celastrol delayed disease onset, improved motor deficits, and increased the number of neurons, promoted Hsp70 expression, and reduced TNF-α and iNOS levels in the spinal cord (Kiaei et al., 2005). Here, SOD1 is linked to amyotrophic lateral sclerosis.