For example, a study combining fMRI with electrophysiology identified that entorhinal cortex hyperactivity in APOE E4 mice, in the absence of overt AD pathology, was associated with decreased response to inhibitory GABAergic inputs on pyramidal neurons, rather than increased excitability due to differences in NMDA glutamate receptors (Nuriel et al., 2017). This evidence concerns the gene APOE and Alzheimer disease.