Ursula Quitterer calls it "Compound 10," a chemical substance developed by her research team that could potentially slow the progression of Alzheimer's disease. Quitterer, Professor of Molecular Pharmacology at ETH Zurich, has so far tested the experimental treatment in mice. The results were encouraging.
The nerve cell death typically associated with dementia slowed significantly, and the treated animals lived longer. The work behind the compound began nearly 20 years ago, when Quitterer received brain tissue samples from patients treated by a doctor and colleague at Ain Shams University Hospital in Cairo. The tissue had been removed during tumor surgery from people with dementia as well as non-dementia patients.
A New Drug Target in Alzheimer's Disease Quitterer used those samples to investigate an enzyme called GRK2, which has long been a major focus of her research. GRK2 plays an important regulatory role in many human cells. It helps cells respond appropriately to signals, stress, and strain.
The enzyme is active in organs including the heart and the brain, where it helps support normal nerve cell function. By analyzing the Cairo tissue samples at the molecular level and conducting experiments in mice, Quitterer and her colleagues uncovered evidence that GRK2 plays an important role in dementia. Their findings were recently published in the journal Cell Reports Medicine.
GRK2 exists in cells in two forms. One is normal and functional, while the other has been inactivated by cellular metabolism. Quitterer's team found unusually large amounts of the inactive form in brain tissue from people with dementia.
The researchers observed the same pattern in mice, specifically in a mouse model for Alzheimer's disease. They also discovered that inactive GRK2 can clump together inside brain cells during dementia. These aggregates collect on mitochondria (the "powerhouses" of the cells), where they can interfere with normal function and cause damage.
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