PGE2 is known to be a potent proinflammatory mediator that is increased in postmortem brain tissue, cerebrospinal fluid, and serum from patients with sporadic ALS [6, 29] and in both the cerebral cortex and spinal cord in the G93A mutant SOD1 transgenic mouse model of ALS [7, 30]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.