GRK2 and Alzheimer disease: The same group went on to report in a transgenic mouse model of AD, where the double-mutant form of APP695 is overexpressed under the regulation of a prion promoter, the overexpression of GRK2, and to a lesser extent GRK5, occurred in the cytosolic versus membrane fractions from hippocampal and cortical brain homogenates with increasing age and plaque deposition.