A Little-Known Protein May Be Fueling Alzheimer’s — and Scientists Found a Way to Block It
A Breakthrough in Alzheimer’s Research: Scientists Identify a New Target Protein and Develop a Promising Treatment
Alzheimer’s disease is a complex and debilitating condition that affects millions of people worldwide. While existing treatments can delay its progression, they do not provide a cure. However, a team of scientists from ETH Zurich has made a groundbreaking discovery that could potentially change the course of Alzheimer’s research.
Ursula Quitterer, Professor of Molecular Pharmacology at ETH Zurich, and her team have identified a little-known protein called GRK2 as a key player in the development of Alzheimer’s disease. GRK2 is an enzyme that plays a crucial role in many human cells, helping them respond to signals, stress, and strain. However, in people with Alzheimer’s, GRK2 becomes inactivated and forms aggregates that interfere with normal cell function and cause damage.
Quitterer’s team discovered that GRK2 exists in two forms: a normal, functional form and an inactive form. They found that people with Alzheimer’s have unusually large amounts of the inactive form in their brain tissue. In mice, the researchers observed the same pattern, with the inactive form of GRK2 clumping together inside brain cells and interfering with normal function.
The team’s research also revealed that the inactive form of GRK2 can increase the production of amyloid beta, a protein fragment considered a main cause of Alzheimer’s. This process creates a vicious circle, where amyloid beta places additional stress on nerve cells, leading to the formation of more inactive GRK2 and GRK2 aggregates.
To interrupt this process, Quitterer and her colleagues created several chemical compounds and tested them in cell cultures and mice. One of the compounds, dubbed Compound 10, stood out as particularly effective. It prevented GRK2 molecules from forming aggregates, allowing mitochondria to function better and reducing the accumulation of amyloid beta.
The effects of Compound 10 were not limited to the brain. In mice, the compound also had a positive effect on heart function and aging processes, with older animals developing fewer grey hairs. These findings suggest that interfering with GRK2 aggregation may influence more than just Alzheimer’s-related processes.
While Compound 10 has shown promise in preclinical trials, it has not yet been developed into a treatment for humans. Quitterer and her team are now searching for a company to partner with to move the compound toward the next stages of drug development.