Considering this, plus a recent description of a frontotemporal dementia variant that displayed reduced glutamate transporter-1 staining in a subset of tau-bearing astrocytes [21], and also that the sole presence of tau in astrocytes in a mouse model for tauopathies produces a significant decrease in glutamate transport capacity [17]; we can speculate that the decrease in synaptic markers observed in the Tg-FDD mouse model could be due to astrocytic dysfunction triggered by tau oligomers. The gene discussed is SLC1A2; the disease is frontotemporal dementia.