There are five EAATs in the human CNS (EAAT1-EAAT5). EAAT2, primarily associated with astrocytes, is the main regulator of extracellular glutamate levels (Danbolt, 2001 and Williams et al., 2005). Loss of EAAT2 protein and defective glutamate transport have been reported in AD (Li et al., 1997 and Masliah et al., 1996), suggesting that decreased activity of glutamate transporters may play a role in the pathogenesis of AD. In contrast, other studies have demonstrated no clear correlation of the levels of glutamate transporters with AD, and have shown that AD cases may contain either normal or reduced EAAT1 and EAAT2 levels (Beckstrom et al., 1999).