During hypoxic-ischemic injury, GRK2 was shown to exacerbate brain damage via p38-dependent TNFα production [83], regulate the metabotropic glutamate receptor function and expression implicated in the pathogenesis of AD and MS, and cause neurodegeneration via the over-activation of group I mGLuTs [110,111]. This evidence concerns the gene GRK2 and Alzheimer disease.