SOD1 and amyotrophic lateral sclerosis: Similarly, in the spinal cord of the G93A-SOD1 transgenic mice that overexpress mutated human G93A-SOD1 protein and recapitulate many pathological hallmarks of ALS, CB2R mRNA, CB2R binding and CB2R levels were upregulated in a temporal pattern closely following disease progression, whereas changes in CB1R expression were not found [237,238].