Interestingly, no such loss was observed in GluN1 NMDARs (control: 0.97 ± 0.12 A.U., Mod-AD: 0.64 ± 0.13 A.U., two-tailed t-test, t = 1.875, P = 0.853, Fig. 1C), which is consistent with the widely accepted role NMDARs play in the pathophysiology of Alzheimer’s disease (Wang and Reddy, 2017). The gene discussed is GRIN1; the disease is early-onset autosomal dominant Alzheimer disease.