Consistent with this concept, mGluR5 selective antagonists improve the cognitive deficits observed in AD mouse models and the genetic deletion of mGluR5 results in a reduction in both soluble Aβ42 oligomers and β-amyloid plaques and results in the amelioration of cognitive dysfunction observed in APPswePSIΔE9 AD transgenic mice [11]. Here, GRM5 is linked to amyloidosis.