Alzheimer’s disease gradually steals memories, independence, and quality of life from millions of people worldwide.
Despite decades of research, scientists still struggle to find treatments that can stop the disease from progressing. Most available medications provide only modest benefits and cannot fully prevent the loss of brain cells that characterizes the condition.
A new study from ETH Zurich may offer a promising new direction. Researchers have developed an experimental compound called Compound 10 that appears to protect nerve cells, improve cellular energy production, and slow processes associated with Alzheimer’s disease in mice. The findings were published in Cell Reports Medicine.
The research began almost 20 years ago when Professor Ursula Quitterer received brain tissue samples from colleagues in Egypt.
Some samples came from people diagnosed with dementia, while others came from patients without dementia. By comparing the tissues, the researchers hoped to identify molecular differences that might help explain why brain cells die during Alzheimer’s disease.
Their attention soon turned to a protein called GRK2. In healthy brains, this protein contributes to the normal functioning of nerve cells. As the team studied the tissue samples, they noticed that many dementia patients had unusually high levels of an inactive form of GRK2.
The problem became even more serious when researchers discovered that inactive GRK2 molecules tended to cluster together. These clusters accumulated inside brain cells and interfered with mitochondria, which are responsible for generating energy.
The researchers found that GRK2 aggregates reduced the ability of mitochondria to generate energy. This appeared to create conditions that encouraged the progression of Alzheimer’s disease. At the same time, the inactive GRK2 protein increased production of amyloid beta, creating a self-perpetuating cycle of damage.
To interrupt this process, the scientists developed a series of experimental compounds. Among them, Compound 10 produced the strongest results. The compound prevented inactive GRK2 molecules from clumping together. As a result, mitochondria functioned more normally, amyloid beta accumulation decreased, and nerve cells remained healthier.
Unexpectedly, researchers also observed benefits beyond the brain. The treated mice showed healthier heart function and signs of slower aging. The next challenge is finding partners willing to support the lengthy process of drug development and human testing.
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Source: ETH Zurich.
