A molecule known simply as "Compound 10" slowed the loss of nerve cells and extended survival in mice with Alzheimer's-like disease, according to work from Ursula Quitterer, Professor of Molecular Pharmacology at ETH Zurich. Her team developed the chemical to block GRK2, an enzyme that has been a central focus of her laboratory for years and that she suspects plays a role in driving the disease.
The trail leading to the compound started almost two decades ago, when Quitterer obtained brain tissue from a physician colleague at Ain Shams University Hospital in Cairo. The samples had been removed during tumor surgery from patients with dementia and from patients without it, giving her a way to compare the two groups and examine what GRK2 was doing in human brain tissue rather than only in animal models.
What makes the result notable is the target itself. Most high-profile Alzheimer's drug development has revolved around amyloid and tau. An enzyme like GRK2 opens a different line of attack, and one that in these experiments affected the outcome that matters most to families - how quickly brain cells are lost, and how long the animals survived.
The important qualifier is that this is a mouse study of an experimental compound, not a treatment available to patients. Many drugs that protect neurons in rodents fail to do so in people, and the path from a laboratory molecule to human trials is long. Still, nearly twenty years of groundwork on a relatively little-studied enzyme has produced something concrete enough to test.