Resulting neuroinflammation may likely explain synapse loss and cognitive deficits.48 Interestingly, in a previous study evaluating the consequences of neuronal overexpression of A2AR in a tauopathy model, the transcriptomic analysis also uncovered a microglial-related response.27 However, despite the upregulation of microglial-selective genes in both APP/PS1 and tau transgenic mice overexpressing A2AR, no overlap could be observed. Here, ADORA2A is linked to tauopathy.