The Pathological Form of Alpha-Synuclein and Its Role in Parkinson’s Disease

The pathological form of the brain protein causes the death of dopamine-rich brain cells

Posted on 12.21.2023 at 8.00pm Views 391 Posted on 12.21.2023 at 8.00pm Modified 12.21.2023 4.18pm Views 391

The death of brain cells and decreased levels of dopamine are considered to be the causes of Parkinson’s disease. Dopamine serves as an important chemical messenger in the brain. As Parkinson’s disease progresses, dopamine-rich nerve cells are increasingly lost. [사진= 게티이미지뱅크]A new clue has been discovered about how the death of dopamine-rich brain cells occurs, which is believed to cause the degenerative neurological disease Parkinson’s disease. Animal experiments have shown that a pathological form of a brain protein called alpha-synuclein combines with other factors to cause brain cell death. This is what the health and medicine webzine ‘Health Day’ reported on the 20th (local time), based on an article by researchers from Johns Hopkins University, USA, recently published in Science Translational Medicine.

The death of brain cells and decreased levels of dopamine are considered to be the causes of Parkinson’s disease. Dopamine serves as an important chemical messenger in the brain. As Parkinson’s disease progresses, dopamine-rich nerve cells are increasingly lost. As a result, motor and cognitive skills continue to deteriorate, leading to various symptoms such as tremors, stiffness and balance disorders. Parkinson’s disease patients usually replace lost dopamine by giving drugs such as L-dopa, a precursor to dopamine, but the effect disappears over time.

A research team led by Professor Ted Dawson (neurology) of Johns Hopkins University has discovered through animal experiments that a pathological form of alpha-synuclein, a common brain protein, may play a role in the death of dopamine-rich brain cells. Although it was assumed that alpha-synuclein was involved in the loss of dopamine-rich brain cells, its role, until now unclear, has now been clarified in a concrete way.

The researchers used cutting-edge technology to identify other proteins that can interact with alpha-synuclein and lead to brain cell death. The researchers discovered 100 candidate substances through laboratory and mouse experiments. Most of them involved cells making new proteins.

When the “bad” form of alpha-synuclein binds to another cellular protein called crystalline sclerosis complex 2 (TSC2), which causes benign tumors to grow within the cell, it causes a third protein called mTOR come into play within the cell. The researchers explained that mTOR promotes protein production within cells, but if its activity becomes excessive it can lead to brain cell death.

The mechanism by which this occurs has not yet been clearly identified. Perhaps the protein interferes with activities within the cell or, when a specific protein is produced in excess, it can become toxic.

However, the researchers found that administering an mTOR-targeting drug called rapamycin to mice with a Parkinson’s disease-like condition blocked excessive production of cellular proteins. The researchers found that mice treated in this way began to lose the “slow and often interrupted movements” characteristic of Parkinson’s disease.

Rapamycin is already used to suppress rejection reactions that can occur after anticancer drugs or organ transplants. However, it comes with serious side effects. So researchers hope that one day a drug like rapamycin can be developed that can keep dopamine-rich brain cells alive with fewer systemic side effects in patients.

Around 10 million people worldwide suffer from Parkinson’s disease. “Parkinson’s disease has a profound impact not only on the quality of life of patients, but also on their carers and loved ones,” Professor Dawson said. “Our research could lead to a mechanical, molecular-based treatment that can actually slow or halt the progression of Parkinson’s disease.” “I hope we deliver that,” he said.

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Journalist Han Geon-pil

hanguru@kormedi.com

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