Nevertheless, the seminal study by Stritmatter and colleagues provides evidence that mGluR5 plays an integral role in regulated Aβ oligomer pathology, as the deletion of mGluR5 expression reduced Aβ oligomer-mediated synapse loss and mGluR5 antagonist (MTEP) treatment results in the amelioration of cognitive deficits normally observed APPswePS1ΔE9 mice at 9 months of age [9]. The gene discussed is GRM5; the disease is cognition.