Scientists have found a new trigger for Alzheimer's disease

Researchers from the Swiss Higher Technical School of Zurich have discovered that the accumulation of an inactive form of the GRK2 protein may be a key factor in the development of Alzheimer's disease. This was reported on June 8 by Science Daily magazine.

Experts examined brain tissue samples obtained from the Ain Shams University Hospital in Egypt. The study showed that the GRK2 protein, which normally supports the functioning of nerve cells and the heart, begins to accumulate in the brains of people with dementia when it becomes inactive. Similar processes have been recorded in experiments on mice.

Scientists have found that inactive GRK2 protein molecules clump together inside nerve cells. These aggregates attach to the mitochondria — the energy centers of cells — and disrupt their work.

The team also found that the accumulation of inactive GRK2 increases the production of beta-amyloid, a protein fragment traditionally associated with Alzheimer's disease. According to scientists, the process turns into a vicious circle: the accumulation of beta-amyloid creates additional stress for neurons, which provokes the formation of even more defective protein GRK2 and accelerates the progression of the disease.

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On May 31, Science Daily reported the discovery of a molecular switch of inflammation in Alzheimer's disease. According to scientists, the STING protein is normally responsible for early warning of threats, but in Alzheimer's disease it undergoes a modification such as S-nitrosylation. It was clarified that after the modification, STING begins to combine into large complexes that trigger the inflammatory process.