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Accordingly, the control of extracellular levels of glutamate dictates its physiological/pathological actions and this equilibrium is maintained primarily by the action of glutamate transporters (such as GLAST, GLT1, and EAAC1) located on astrocytic cell membranes, which remove the excitatory neurotransmitter from the synaptic cleft, keeping its extracellular concentrations below toxic levels (Anderson and Swanson, 2000

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While the initiating, etiologic agent(s) are not known, the supporting science indicates that the development and progression of the disorder involve inadequacies of GSH