Importantly, inhibiting the expression of Hsa21-encoded type I interferon receptor genes (IFNARs) improves the defective DS microglia functions during brain development and prevents DS microglial senescence in response to pathological tau, suggesting that new therapeutic strategies targeting IFNARs could prevent human microglial senescence to potentially slow the progression of AD in DS. The gene discussed is MAPT; the disease is Alzheimer disease.