This clearance is primarily regulated by the excitatory amino acid transporter 2 (EAAT2) expressed by astrocytes, and reductions in EAATs have been observed in a SOD1 mouse model of ALS as well as in the post-mortem cortical and spinal cord tissues of fALS and, to a greater extent, sALS patients (Rothstein et al., 1995; Trotti et al., 1999; Vucic and Kiernan, 2013; King et al., 2016). Here, SOD1 is linked to amyotrophic lateral sclerosis.