While there are important limitations of hAPP/Nptx2-/- mice as a model of AD including supra pathophysiological levels of Aß and complete deletion of NPTX2, these studies identify GluA4 expression and effects on inhibitory circuit function as consequences of the combined action of amyloidosis and NPTX2 down-regulation. The gene discussed is NPTX2; the disease is Alzheimer disease.