In contrast, NgR-deficient AD mice reduced amyloid burden and improved cognitive impairment.147 BACE-1 inhibition in microglia facilitated the microglia phenotype transition from homeostatic to stage 1 disease-associated microglia (DAM-1) signature148 and thus enhanced amyloid clearance and improved cognitive performance in AD mice.149 In addition, microglia interact with astrocytes to promote Aβ clearance. The gene discussed is BACE1; the disease is Alzheimer disease.