Researchers at ETH Zurich have developed an active ingredient that interrupts a self-reinforcing process in Alzheimer’s disease. In treated mice, dementia progressed much more slowly and the animals survived longer.

The core of the research is the body’s own enzyme GRK2, which acts as a regulatory protein in cells. As the team led by Ursula Quitterer, Professor of Molecular Pharmacology at ETH Zurich, discovered, an inactivated form of this enzyme accumulates in Alzheimer’s patients and in corresponding mouse models. This forms clumps that accumulate on mitochondria, damaging them and leading to cell stress. In addition, the inactive form promotes the production of beta-amyloid, the central protein in Alzheimer’s disease. Beta-amyloid, in turn, increases stress, which leads to more inactive GRK2 – a vicious cycle that promotes the progression of the disease.

The researchers developed several compounds to break this cycle. “Compound 10” proved to be particularly effective. The substance prevents GRK2 from clumping, improves mitochondrial function, reduces beta-amyloid deposition and protects nerve cells from dying.

In addition to the effects in the brain, the scientists also observed positive effects on heart function and aging processes in the mice, including less gray hair formation.

The basic research, which began almost 20 years ago with brain tissue samples from Cairo, has now been published in the journal “Cell Reports Medicine”. Substance 10 has been applied for a patent. Quitterer and ETH Zurich are now looking for an industrial partner for the further development of a potential drug.

Alzheimer’s is a complex disease, Quitterer emphasized. Previous drugs could only delay the course by a few months. The new approach via GRK2 works via a different mechanism and could be used in combination with other therapies in the future.

Original Paper:

Abd Alla J, Perhal A, Fu X, Langer A, el Faramawy Y, Quitterer U: Analysis of GRK2 aggregation in the pathology of Alzheimer disease in animal models. Cell Reports Medicine 2026, 7: 102707, DOI: 10.1016/j.xcrm.2026.102707

Editor: X-Press Journalistenbüro GbR

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