Genetic deletion of P2X7R in APP/PS1 mice improved long-term synaptic plasticity, spatial learning and memory dysfunction relative to wild-type littermates [71], and P2X7R antagonism in mouse models of tauopathy harbouring the frontotemporal dementia (FTD)-causing MAPT mutations G272V and/or P301S ameliorates cognitive and behavioural deficits as well as synaptic dysfunction [72,101,136]. Here, APP is linked to tauopathy.