Alzheimer’s disease is one of the greatest medical challenges of our time. Millions of people around the world live with the condition, and the number continues to grow as populations age. The disease slowly destroys memory, thinking abilities, and independence.
Although several drugs have been developed in recent years, most only slow the disease for a limited time and do not stop the underlying damage occurring inside the brain.
Now, researchers at ETH Zurich have identified a promising new target that may open the door to a different way of treating Alzheimer’s disease. Their findings, published in Cell Reports Medicine, describe a newly developed experimental compound that protected brain cells in mice and appeared to slow several processes linked to aging.
The story behind the discovery began nearly two decades ago. Professor Ursula Quitterer, a molecular pharmacologist at ETH Zurich, received brain tissue samples from colleagues at Ain Shams University Hospital in Cairo.
These samples came from patients who had undergone brain surgery. Some patients had dementia, while others did not. The researchers hoped that studying these tissues might reveal hidden clues about what happens inside the brain during Alzheimer’s disease.
At the center of the investigation was a protein called GRK2. This protein is found throughout the body and plays an important role in helping cells respond to signals, stress, and changing conditions. GRK2 is active in many organs, including the heart and brain. In healthy nerve cells, it helps maintain normal cellular function.
When the researchers analyzed brain tissue from dementia patients, they discovered something unusual. GRK2 existed in two forms. One form was active and functioning normally. The other form had been chemically altered and no longer worked properly. This inactive form appeared in much larger amounts in the brains of people with dementia.
Further experiments in mice revealed an important problem. The inactive GRK2 molecules tended to stick together and form clumps. These aggregates accumulated inside brain cells and attached themselves to mitochondria, the structures responsible for producing energy.
Mitochondria are often called the powerhouses of cells because they generate the energy needed for survival. When GRK2 aggregates interfered with these structures, energy production dropped. The cells became stressed and less able to function normally.
The researchers also discovered another troubling effect. Inactive GRK2 appeared to increase the production of amyloid beta, a protein strongly linked to Alzheimer’s disease. This created a vicious cycle that could contribute to disease progression.
To break this destructive process, the researchers developed several experimental compounds. After extensive testing in laboratory cells and mice, one candidate stood out. The team named it Compound 10.
Compound 10 prevented GRK2 molecules from forming harmful aggregates. As a result, mitochondria functioned more effectively, energy production improved, and amyloid beta accumulation decreased. Most importantly, nerve cells survived longer and maintained their function.
If you care about Alzheimer’s, please read studies about the likely cause of Alzheimer’s disease , and new non-drug treatment that could help prevent Alzheimer’s.
For more health information, please see recent studies about diet that may help prevent Alzheimer’s, and results showing some dementia cases could be prevented by changing these 12 things.
Source: ETH Zurich.
