A team at ETH Zurich has produced an experimental substance that slows the progression of Alzheimer's-type symptoms in mice. Ursula Quitterer, Professor of Molecular Pharmacology at ETH Zurich, calls it "compound 10." In the animal tests reported so far, the loss of nerve cells characteristic of dementia proceeded significantly more slowly, and the treated mice lived longer. The researchers also observed anti-aging effects from the substance.
The target is an enzyme called GRK2, which has been the focus of Quitterer's work for years. GRK2 is a regulatory protein that helps cells respond appropriately to signals, stress and strain. It is active in the heart and also in the brain, where it supports the functioning of nerve cells - which is what makes it an interesting handle for a drug aimed at protecting neurons rather than clearing plaques.
The project traces back nearly two decades, to brain tissue samples that Quitterer received from a colleague at the Ain Shams University Hospital in Cairo. The samples had been removed during tumor surgery from both patients diagnosed with dementia and patients without dementia, giving the team a direct comparison in human tissue to work from.
What has been shown so far is a result in mice, not in people, and the substance has not been tested in Alzheimer's patients. Compounds that protect neurons in rodents frequently fail to reproduce those benefits in humans, so the practical question is whether compound 10 can move into human testing and hold up there. For now, it adds to a line of research pursuing nerve cell protection as an alternative angle on a disease that has proved stubbornly resistant to treatment.