A little-known protein may be fueling Alzheimer’s — and scientists found a way to block it
An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup. The treatment also appeared to improve heart health and slow some signs of aging, raising hopes for an entirely new way to combat dementia.
Professor Ursula Quitterer from ETH Zurich has developed a potential new treatment for Alzheimer's disease, dubbed "Compound 10." This compound was inspired by her 20-year study of an enzyme called GRK2, which she discovered plays an important role in dementia. Quitterer and her team examined brain tissue samples from patients with and without dementia, finding unusually high amounts of inactive GRK2 in those with the disease.
They also observed that inactive GRK2 forms aggregates inside brain cells, interfering with normal function and potentially causing damage. These aggregates also block mitochondrial pores, reducing energy production within cells and causing stress. This stress, in turn, increased the production of amyloid beta, a protein fragment associated with Alzheimer's.
Compound 10 blocks GRK2 molecules from forming these aggregates, allowing mitochondria to function better and reducing amyloid beta accumulation. In mice experiments, Compound 10 led to slower nerve cell death, longer life, and improved heart function, as well as fewer grey hairs. While these findings are promising, Compound 10 is still in preclinical stages and has not yet been developed into a treatment for humans.
The researchers are currently seeking a partner to help advance the compound through the drug development process.
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