Similarly, a study of AD conducted on different mouse models at different ages found an upregulation of IFN-I response genes, together with early memory decline and a progressive accumulation of Aβ [80,83], while the genetic ablation of Cgas in a mouse model of tauopathy reduced the microglial IFN-I response, preserved synapse integrity, and improved cognitive impairment [84]. The gene discussed is CGAS; the disease is Cognitive impairment.