SOD1 and amyotrophic lateral sclerosis: While the heterozygous SOD1 (G93A) P2X7 receptor+/− animal model did not present any significant differences in body weight, disease onset, or motor performance, the genetic deletion of P2X7 receptor expression (P2X7−/−), instead of improving ALS disease conditions, accelerated disease onset and progression, induced neuroinflammatory responses, and produced MNs depletion at end stages of the disease in comparison with P2X7+/+/SOD1 (G93A) animals (Apolloni et al., 2013a).