A New Alzheimer’s Target Emerges
ETH Zurich researchers have reported early findings on an experimental Alzheimer’s treatment that targets a cellular process not addressed by current drugs. The compound, called Compound 10, was developed during nearly two decades of work led by Ursula Quitterer, a professor of molecular pharmacology at ETH Zurich.
The research began with human brain tissue samples provided by Ain Shams University Hospital in Cairo from people with and without dementia. Those samples helped the team investigate GRK2, a regulatory protein involved in cellular signaling and stress responses in organs including the brain and heart.
In findings published in Cell Reports Medicine, the researchers report that an inactive form of GRK2 builds up in the brains of people with dementia and in mice with Alzheimer’s-like symptoms. The inactive proteins appear to form aggregates inside nerve cells and attach to mitochondria, interfering with the cells’ energy production. The team also found evidence that inactive GRK2 may increase amyloid beta, a protein fragment associated with Alzheimer’s disease. This may create a cycle in which amyloid beta stresses nerve cells, leading to more inactive GRK2 and further damage.
Compound 10 was designed to interrupt that cycle. In cell studies and mouse experiments, it reduced GRK2 aggregation, improved mitochondrial function, lowered amyloid beta deposits, and slowed nerve cell loss. Treated mice also lived longer, showed signs of improved heart function, and developed fewer gray hairs as they aged.
The results remain preliminary. The compound has not yet been tested in humans, and the researchers are seeking an industry partner to advance development. Quitterer said Alzheimer’s research is slow partly because studies require older animals and long observation periods.
If further research supports the findings, Compound 10 could represent a new treatment approach, potentially used alongside existing medications to slow disease progression.