# Experimental drug blocks a hidden Alzheimer’s trigger in mice

> Researchers at ETH Zurich have identified a new Alzheimer's disease target and developed an experimental compound that slowed nerve cell loss in mice. The work centers on GRK2, a regulatory protein that can form damaging clumps inside nerve cells when it becomes...

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Byline: ETH Zurich
Published: 2026-07-11T21:05:30+00:00
Categories: Health, News

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Researchers at [ETH Zurich](https://ethz.ch/en/news-and-events/eth-news/news/2026/06/new-drug-could-slow-the-development-of-alzheimers.html) have identified a new Alzheimer's disease target and developed an experimental compound that slowed nerve cell loss in mice. The work centers on GRK2, a regulatory protein that can form damaging clumps inside nerve cells when it becomes inactive.

The compound, called **Compound 10** by the research team, acted on a disease process that existing Alzheimer's drugs leave largely untouched. In mouse studies, it helped protect neurons, reduced Alzheimer's-related changes and extended survival. The research was published in **Cell Reports Medicine**.

The findings are still early. Compound 10 has been tested in cells and mice, rather than in people. Even so, the ETH Zurich team says the results point to a possible new treatment path for a disease that remains difficult to slow.

## A new target in Alzheimer's disease

The research grew from an unusual scientific thread that began almost two decades ago. **Ursula Quitterer**, Professor of Molecular Pharmacology at ETH Zurich, received brain tissue samples from a colleague at Ain Shams University Hospital in Cairo. The samples had been removed during tumor surgery and came from people with dementia as well as people without dementia.

Those samples helped guide the team toward **GRK2**, short for G protein-coupled receptor kinase 2. This protein helps cells respond to signals and cope with stress. It is active in the brain and heart, where stable signaling and energy balance are essential for healthy function.

In the new study, the researchers found that GRK2 can become inactive and accumulate in the brains of people with dementia. Similar patterns appeared in mouse models that develop Alzheimer's-like disease. That made GRK2 more than a background player in the team's view. It became a possible driver of damage.

This matters because Alzheimer's disease has long been linked to changes such as amyloid beta buildup and nerve cell death. The ETH Zurich study adds another layer. It suggests that the form and behavior of GRK2 may influence how those harmful changes unfold inside brain cells.

## How GRK2 disrupts brain cells

Inside neurons, the inactive form of GRK2 can gather into **protein aggregates**. These clusters appear to interfere with mitochondria, the tiny structures that provide much of the energy cells need. Neurons are especially sensitive to energy stress because they have high demands and limited room for failure.

The ETH Zurich team found that inactive GRK2 aggregates attach to mitochondria and disturb their function. When mitochondria struggle, nerve cells face a growing energy shortage. That stress can push cells closer to degeneration and death.

The researchers also observed a connection between inactive GRK2 and **amyloid beta**, the protein fragment strongly associated with Alzheimer's disease. In their experiments, inactive GRK2 appeared to promote amyloid beta production. More amyloid beta then increased stress on neurons, which helped create conditions for further GRK2 inactivation and aggregation.

This cycle gives the study much of its force. A damaged stress-response protein may help drive mitochondrial problems. Those problems may feed amyloid-related stress. The process can then reinforce itself inside vulnerable brain cells.

For general readers, the key point is straightforward. The ETH Zurich researchers traced a possible chain of damage from an altered protein to failing cellular energy production and then to a familiar Alzheimer's marker. That chain offered a target for intervention.

## Compound 10 breaks the damaging cycle

To test that target, the researchers designed and screened chemical compounds that could interfere with harmful GRK2 aggregation. **Compound 10** emerged as the strongest candidate in their experiments. It prevented GRK2 molecules from forming damaging clusters and helped mitochondria work more effectively.

In mouse models of Alzheimer's disease, the effects extended across several signs of decline. The treated animals showed slower nerve cell death. They also had reduced amyloid beta deposits and lived longer than untreated mice in the study.

The compound appeared to help outside the brain as well. The ETH Zurich announcement says the treated mice showed improved heart function. Researchers also observed fewer gray hairs as the animals aged, which points to broader effects on aging-related changes in this mouse model.

These findings make Compound 10 scientifically intriguing, while keeping the next steps clear. A result in **mouse models** can reveal a promising mechanism and help guide drug development. Human biology brings additional hurdles, including safety, dosing, delivery and long-term effects.

Still, the approach is notable because it acts through GRK2. Current Alzheimer's medications can offer limited delays in progression for some patients. A future therapy that targets a separate mechanism could one day be tested alongside other approaches, if development proceeds successfully.

## Why the work took nearly 20 years

Alzheimer's research often moves slowly because the disease develops over long periods. The ETH Zurich team worked with older mice, usually between one and a half and two years old. Each experiment required enough time for age-related disease processes to appear and for treatment effects to become meaningful.

Quitterer described the pace directly. "It took so long simply because everything takes so long in Alzheimer's research," she said.

That slow timeline shaped the entire project. A single experiment could take many months before the team knew whether a finding was strong enough to justify the next step. The need to study aging animals also limited how quickly experiments could be repeated or expanded.

Quitterer added, "It's all a great deal slower than in cancer research, for example." The comparison highlights a practical challenge. Diseases that unfold with aging demand patience from researchers and funding systems alike.

The long timeline also explains why the discovery rests on several kinds of evidence. The team used human brain tissue, molecular analyses, cell studies and animal experiments. Together, those approaches allowed the researchers to connect GRK2 aggregation with Alzheimer's-like pathology and then test whether blocking that aggregation could help.

## What comes before human trials

The ETH Zurich team has completed the basic research phase and filed a patent application for **Compound 10**. The researchers and university are now seeking a company interested in moving the compound toward drug development.

That next stage would require extensive work. Before any human trial, researchers would need to refine the compound, study how it behaves in the body and test safety in additional preclinical systems. They would also need to determine whether the compound reaches the brain in useful amounts.

Quitterer stressed the difficulty of the disease. "Alzheimer's is a very complex disease," she said. That complexity is one reason a single target rarely solves every part of the condition. Alzheimer's involves many interacting changes, including protein buildup, inflammation, cellular stress and widespread loss of neural connections.

The promise of the new study lies in its fresh target. By focusing on **inactive GRK2** and mitochondrial stress, the research opens a route that differs from amyloid-centered strategies. If future studies support the finding, GRK2 could become a useful target for drug development.

For now, Compound 10 remains an experimental compound with encouraging results in mice. The ETH Zurich work gives scientists a clearer view of one damaging pathway and a possible way to interrupt it. The path to a treatment for patients will require careful testing, industry partnership and time.