It has been previously reported that inactivation of A2AR influenced the phosphorylation level of GSK-3β at Ser9 markedly in a mouse model of tauopathy.22 On the basis of the fact that the influences of GSK-3β on the hyperphosphorylation of tau have been well demonstrated, our present study provides strong evidence for the A2AR activation-induced tau phosphorylation and the resulting neurological dysfunction after TBI. Here, ADORA2A is linked to tauopathy.