We also observed that deletion of Tyrobp in a tauopathy mouse model reduced the expression of C1q and improved learning behavior and synaptic function despite a paradoxical increased in the spread and the phosphorylation state of tau [61]. The regulation of the complement subnetwork by TYROBP, including a decrease in several of the same components previously reported further supports a beneficial effect of decreased complement pathway activation in AD pathology. The gene discussed is TYROBP; the disease is Alzheimer disease.