Researchers at ETH Zurich, led by Professor Ursula Quitterer, report findings in the journal Cell Reports Medicine. The work began almost 20 years ago when Quitterer received brain tissue samples from surgeries in Cairo. The team analysed human tissue and ran experiments on mice to study an enzyme called GRK2, which helps cells respond to signals and supports nerve cell function.
They found two forms of GRK2: a normal functional form and an inactivated form produced by metabolism. The inactivated form is abundant in dementia patients' brain tissue and in a mouse model for Alzheimer’s. Inactive GRK2 aggregates on mitochondria, blocks mitochondrial pores, lowers available energy and raises cellular stress. It also promotes amyloid beta production, creating a self-perpetuating cycle of stress and aggregation.
To break this cycle, the team developed chemical compounds and tested them in cell cultures and older mice. Compound 10 prevented GRK2 aggregation, improved mitochondrial function, reduced amyloid beta deposits and supported nerve cell survival. Mice also showed better heart function and signs of slower ageing, such as fewer grey hairs. The researchers have applied for a patent, consider the basic research complete, and are seeking a company to develop the compound further.
Difficult words
- enzyme — protein that speeds up chemical reactions
- aggregation — process where parts form a group or clump
- mitochondrion — cell structures that make energy for the cellmitochondria
- amyloid beta — protein fragment linked to Alzheimer’s disease
- metabolism — chemical processes that keep a cell alive
- compound — a chemical substance made for testscompounds, Compound 10
- patent — legal right to protect an invention
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Discussion questions
- What are the possible benefits for patients if a compound prevents GRK2 aggregation?
- Do you think using mice in this research is acceptable? Why or why not?
- What challenges might researchers face when moving from mouse tests to treatments for people?
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