APP and Alzheimer disease: This model avoids artifactsassociated with APP overexpression and thus better replicates thehuman AD pathophysiology compared to models that overexpress APP.The App knock-in mice exhibit robust Aβ pathology,neuroinflammation, synaptic loss, and memory impairment. Here, using whole-cell patch-clamp recordingsof synaptically activated glutamate transporter currents (STC) inastrocytes, we report that glutamate transporter function in hippocampal AppNL‐G‐F mouseastrocytes is impaired, as reflected by the slow rate of glutamateclearance following synaptic stimulation of primary astrocytes.