Scientists at ETH Zurich have developed a chemical compound that significantly slows the progression of Alzheimer’s disease in mice, and which they believe could one day be used alongside existing medications to improve quality of life for dementia patients.
The compound, which the research team is calling “Compound 10,” is the result of nearly 20 years of research by Professor Ursula Quitterer, a molecular pharmacologist at ETH Zurich. In mice treated with the substance, the typical death of nerve cells seen in dementia is significantly slower, and the animals survive for longer. The findings have been published in the journal “Cell Reports Medicine.”
Why It Took 20 Years?
The research began when Quitterer received brain tissue samples from a colleague at Ain Shams University Hospital in Cairo, samples removed during tumour surgery from both dementia and non-dementia patients. What she found in those samples set her team on a two-decade path.
“It took so long simply because everything takes so long in Alzheimer’s research,” explains Quitterer.
The glacial pace of the work, she explains, is inherent to the nature of Alzheimer’s research.
Because the disease is age-related, experiments must be conducted on older animals, mice aged one and a half to two years. Each experiment takes that long to complete, and its conclusions must then feed into the design of the next one. “It’s all a great deal slower than in cancer research, for example,” she said.
The Vicious Circle of Dementia
To understand how Compound 10 works, it helps to understand what it targets. At the centre of the research is an enzyme called GRK2, a regulatory protein found throughout the body, including in the brain, where it supports the function of nerve cells.
The ETH Zurich team found that in dementia patients, an inactivated form of GRK2 builds up in abnormally large quantities in brain tissue. This inactivated form clumps into aggregates that attach themselves to the mitochondria (the energy-producing structures inside cells) blocking their pores, reducing their energy output and creating a state of stress within the cell.
That cell stress then triggers increased production of amyloid beta, the protein fragment widely considered a primary driver of Alzheimer’s disease. And crucially, that amyloid beta in turn causes further stress, which generates more inactive, aggregated GRK2. A self-perpetuating loop that accelerates the disease.
Breaking the Loop
Compound 10 interrupts this cycle directly. In cell culture experiments and in mice, the compound prevented GRK2 molecules from forming those damaging aggregates in the first place. With the aggregates absent, mitochondria function better, amyloid beta deposits are reduced, and nerve cells maintain their function rather than dying off.
The researchers also observed unexpected effects outside the brain: Compound 10 had a positive influence on heart function and on ageing processes more broadly. Treated mice developed fewer grey hairs in old age, a striking, if modest, indicator of systemic anti-ageing activity.
Fight Against Alzheimer’s: What Comes Next?
ETH Zurich has applied for a patent on Compound 10, and the basic research phase is now complete. The university and Professor Quitterer are now actively looking for a commercial partner to take the compound through the next stages of drug development, a process that would ultimately require clinical trials in humans before any approved medication could reach patients.
Quitterer is careful about expectations. Current Alzheimer’s medications do not cure the disease, but at most delay its progression by several months. What makes Compound 10 potentially significant, she argues, is not that it replaces those drugs but that it works via a different mechanism, targeting GRK2 rather than amyloid beta directly.
“That’s why it’s so important that we’ve now identified a new target protein in the form of GRK2,” she said.
Used in combination with existing medications, it may one day be possible to meaningfully improve quality of life for patients.
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