At present, we have a poor understanding of how GLT-1 dysfunction in AD alters the spatiotemporal dynamics of glutamate at pre- and postsynaptic membranes, and therefore a poor understanding of the glutamate receptor subtypes, and the side of the synapse on which they reside, that are most heavily impacted by GLT-1 impairment. This evidence concerns the gene SLC1A2 and Alzheimer disease.