Knock down of IRF-1 leads to an increased percentage of internalized GluN1 in primary neuronal cells (Fig. 4A-B), while over-expression of IRF-1 results in a more pronounced surface expression of GluN1, but not GluN2A, or GluN2B in cells (Fig. 4C-D), and in the brains of 3xTg-AD mice (Fig. 4E-F). Here, IRF1 is linked to Alzheimer disease.