To a lesser extent, EAAT2 loss was observed in the occipitaland frontal cortices.106 Complimentarily,in a very recent work it was shown that tau oligomers, following internalizationinto the astrocytic intracellular space, inhibited EAAT2 expressionand decreased the capacity of astrocytes to uptake glutamate.107 These findings suggest that, perhaps, EAAT2dysfunction and reactive astrogliosis are not only associated withAβ pathology in AD but also with pathological tau in the laterstages of the AD continuum. This evidence concerns the gene SLC1A2 and Alzheimer disease.