In vitro studies also showed increased densities of P2X7 and P2X4 receptors, upregulation of P2Y6 receptor expression, and decreased ectonucleotidase CD39 hydrolytic activity in transgenic mice SOD1 (G93A)-derived microglia, all indicating a potentiation of the purinergic system in ALS. Here, SOD1 is linked to amyotrophic lateral sclerosis.