The research was published Oct. 14 in the journal Science Translational Medicine. The paper is titled Loss of GPR3 reduces the amyloid plaque burden and improves memory in the disease mouse models and it details research with mice who were given the protein and developed signs of Alzheimer’s and other dementia.
The GPR3 protein was then eliminated from the mice, who showed memory improvement and other cognitive improvement. Removing GPR3 reduced the amount of amyloid plaque in their brains; it is the build-up of amyloid plaque that is believed to be the cause of dementia.
Researchers also conducted autopsies on the brains of people who died of dementia and they showed a high-level of the GRP3 protein to be present.
The researchers, lead by Dr. Yunhong Huang of the University of Leuven in Belguim, wrote that they seek in part to present “a strong case to convince the pharmaceutical industry to launch a drug development program for Alzheimer’s disease.”
They note some drugs on the market already target the GPR3 protein, also referred to as the G protein-coupled receptor, but say more drug development in this area needs to be done.
They said their research needs to be replicated in humans with Alzheimer’s to verify the role the GRP3 protein plays in the build-up of amyloid plaques and the progression of dementia.
