Scientists found a new Alzheimer’s trigger and a drug that stops it
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- ETH Zurich researchers found that inactive GRK2 protein accumulates and clumps inside nerve cells in dementia patients, blocking pores in mitochondria and starving cells of energy while also driving amyloid beta production
- Compound 10, the team's experimental drug, prevented GRK2 aggregates from forming in mice, allowing mitochondria to function and reducing amyloid beta deposits and nerve cell death
- Treated mice also lived longer, showed improved heart function, and developed fewer gray hairs as they aged, suggesting Compound 10 has anti-aging effects beyond the brain
- Ursula Quitterer, Professor of Molecular Pharmacology at ETH Zurich, led the nearly two-decade investigation, using brain tissue samples originally collected during tumor surgeries at Ain Shams University Hospital in Cairo
- The team has filed a patent application for Compound 10 and is seeking a pharmaceutical company to advance it toward drug development — no human trials have been conducted
- Quitterer noted that current Alzheimer's medications only delay progression by several months and work through different mechanisms, making the GRK2 pathway a potentially complementary target for combination therapy
Why it matters: Current Alzheimer's drugs only delay progression by several months, per Quitterer, and work through mechanisms distinct from the GRK2 pathway. Compound 10 attacks a different driver — protein aggregation that starves nerve cells of energy — and could eventually be combined with existing treatments to extend patient benefits. The broader anti-aging effects observed in mice (fewer gray hairs, better heart function) hint at wider applications, though human testing has not yet begun.
