Importantly, the analogous reduction in GluN1 co-purified with α7 from cortical homogenates from adult 3xTg-AD mice compared to age-matched controls further supports that these reductions may be attributable to specific processes related to amyloidosis and/or tauopathy, in particular in the light of the comparable GluN1/α7 ratios observed in young 3xTg-AD and age-matched controls (Figs 3 and 4). The gene discussed is GRIN1; the disease is Alzheimer disease.