These results are similar to the observed GLT-1 downregulation and neuronal hyperexcitability of AD (Masliah et al., 1996; Rothstein et al., 1996; Kirvell et al., 2006; Jacob et al., 2007; Palop et al., 2007; Bechtholt-Gompf et al., 2010; Mookherjee et al., 2011; Scott et al., 2011; Takahashi et al., 2015). This evidence concerns the gene SLC1A2 and Alzheimer disease.