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). The gene discussed is MAPT; the disease is Alzheimer disease.