Scientists found a new Alzheimer’s trigger and a drug that stops it

Researchers at ETH Zurich have discovered a potential new target for Alzheimer’s disease treatment and developed an experimental compound to address it. Led by Professor Ursula Quitterer, the team identified that an inactive form of the GRK2 protein accumulates in brain cells of Alzheimer’s patients, clumping near mitochondria and impairing energy production. This disruption contributes to nerve cell stress and amyloid beta accumulation, worsening disease progression. The study began two decades ago when Quitterer received brain tissue samples from Ain Shams University Hospital in Cairo, comparing samples from dementia patients and healthy individuals. Using both human tissue and mouse models, the team found that inactive GRK2 molecules form harmful aggregates in nerve cells, blocking mitochondrial function and accelerating cell damage. To combat this, the researchers designed 'Compound 10,' an experimental treatment that prevents GRK2 aggregation. In mouse trials, the compound restored mitochondrial function, reduced amyloid beta deposits, and slowed nerve cell loss. Surprisingly, it also improved heart health and delayed aging-related changes, such as graying hair. The findings, published in *Cell Reports Medicine*, suggest GRK2 plays a dual role in Alzheimer’s, both as a stress regulator and a contributor to neurodegeneration. The team has filed a patent for Compound 10 and plans to advance it toward clinical testing, though further research is needed to confirm its safety and efficacy in humans. Quitterer noted the lengthy timeline of the study reflects the complexity of Alzheimer’s research, emphasizing the need for targeted approaches beyond current treatments. The discovery offers a promising new pathway for therapeutic intervention, potentially addressing both neurological and systemic effects of the disease.