A little-known protein may be fueling Alzheimer’s — and scientists found a way to block it
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- Ursula Quitterer's team at ETH Zurich developed "Compound 10," which in mouse experiments prevented inactive GRK2 from aggregating on mitochondrial pores, slowing nerve cell death and extending the animals' lifespan.
- Analysis of brain tissue samples from dementia patients collected roughly 20 years ago at Cairo's Ain Shams University Hospital revealed unusually large amounts of inactive GRK2 clumping on mitochondria and starving cells of energy.
- Published in Cell Reports Medicine, the work describes a vicious cycle: inactive GRK2 boosts amyloid beta production, and amyloid beta in turn drives more GRK2 to form aggregates inside neurons.
- Beyond the brain, Compound 10 also improved heart function in mice and reduced grey hair in older animals, hinting at broader effects on aging processes that the researchers say warrant further investigation.
- The researchers have filed a patent on Compound 10 and completed the basic research phase; Quitterer and ETH Zurich are now searching for a pharmaceutical company to move the compound into clinical development.
- Quitterer framed the work as complementary: because Compound 10 acts through a mechanism no existing Alzheimer's drug uses, it could potentially be combined with current treatments rather than replace them.
Why it matters: Existing Alzheimer's medications at best delay progression by several months, and Compound 10 attacks GRK2 aggregation on mitochondria—a pathway no current drug touches. Quitterer's team positions it to complement existing treatments, though human trials remain years away and require a pharmaceutical partner the lab is still seeking.
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