Accordingly, it was reported that genetic reduction of GLT-1 levels accelerates the onset of cognitive deficit in a double (AβPPswe/PS1ΔE9) transgenic AD mouse model (Mookherjee et al., 2011), whereas the pharmacological upregulation of GLT-1 ameliorates the pathological tau accumulation, restores synaptic proteins and rescues cognitive decline, with minimal effects on Aβ pathology, in 3xTgAD mice (Zumkehr et al., 2015). Here, SLC1A2 is linked to Alzheimer disease.