GPR3 and Alzheimer disease: A study using a mouse model that altered GPR3 (an orphan G protein-coupled receptor implicated in AD) to be G protein-biased (engineered to favor G protein signaling over β-arrestin pathways by mutation of phosphorylation sites in its C-terminus) demonstrated that this change led to reduced endogenous Aβ40 and Aβ42 production and decreased amyloid plaque area102.