Furthermore, in studies of cellular models of Alzheimer's disease, it was found that in hippocampal cells, GluN2A and GluN2B of astrocytes were able to counteract the synaptotoxic effects of anti‐amyloid beta (Aβ) and that this synaptic protection may be achieved by paracrine secretion of β‐neurotrophic factor.34, 35. The gene discussed is GRIN2A; the disease is early-onset autosomal dominant Alzheimer disease.