The ability of amyloid β to boost extracellular glutamate levels in the hippocampus may be largely attributable to suppressed membrane expression of the GLT-1 glutamate receptor in astrocytes; AD model mice with a concurrent heterozygous deficiency of GLT-1 develop accelerated cognitive dysfunction, whereas, in autopsy studies, patients with significant amyloid plaques tended to be cognitively normal at death when their astrocytes showed higher levels of GLT-1 expression [17,18,19]. Here, SLC1A2 is linked to Alzheimer disease.