Notably,inhibition of Clec7a with Laminarin has been shown to ameliorate memorydeficits in tauopathy mice. Thus, CLEC7Ais already used as a reference microglial marker gene associated withAD. These data suggest the criticalrole of microglial Dectin-1 as a new direct receptor for Aβ42,offering therapeutic strategies for neuroinflammation in AD. Supporting this, studies have shown that negativemodulation of CLEC7A improves microglial activation in AD. Thus, CLEC7A emerges as a therapeutic targetto regulate microglial activation in AD. The gene discussed is CLEC7A; the disease is tauopathy.