SOD1 and amyotrophic lateral sclerosis: Under conditions where SOD1 (G93A) motor neurons are more vulnerable to physiological stress [51] and SOD1 (G93A) glial cells are less able to support motor neuron survival [51], [52], a depleted expression of EAAT2, resulting in elevated glutamate and potential of excitotoxicity, together with glial cell activation and concomitant release of proinflammatory cytokines, described in cellular and animal models of ALS [53], clearly has greater likelihood to impair the function of neighboring motor neurons and induce apoptosis.