Since the glial glutamate transporter-1 (GLT-1) takes the majority of glutamate (account for up to 70%) from synaptic clefts and plays an important role in glutamate homeostasis in the peri-synaptic region (Anderson and Swanson, 2000), modulating the expression and/or function of GLT-1 to increase the glutamate uptake and decrease the glutamate spillover would inhibit the over-activation of Group II mGluRs and contribute to improve the learning, memory, and cognitive deficits in AD. This evidence concerns the gene SLC1A2 and Alzheimer disease.