GRM5 and early-onset autosomal dominant Alzheimer disease: Similarly, in the transgenic APP/PS1 mouse model of Alzheimer’s disease, mGluR5 overexpression has been demonstrated on reactive astrocytes surrounding β-amyloid (Aβ) plaques [207], and in a cell culture system, the binding of (Aβ) oligomers to the astrocytic cell surface triggered the clustering of mGluR5 receptors and a resultant increase in adenosine triphosphate (ATP) release following activation of astroglial mGluR5 by its agonist (DHPG) [207].