Protein studies could pave the way for a new therapy for multiple sclerosis

Researchers in Germany are cautiously optimistic about new therapeutic options for multiple sclerosis after decoding the functions of two key proteins.

Multiple sclerosis (MS) is a disease in which the insulating shells of nerve cells in the brain and spinal cord are damaged. There is no known cure and treatment seeks to improve post-attack function and prevent new attacks.

Nearly 3 million people worldwide suffer from MS.

Juliane Bauch MS study
In her doctorate, Juliane Bauch dealt intensively with the cause of the destruction of myelin sheaths in multiple sclerosis.
RUB, Kramer / Zenger

Now researchers at Ruhr University Bochum have announced a breakthrough in the study of tenascin C and tenascin R proteins.

MS is the most common demyelinating disorder or disorder of the nervous system in which the myelin sheath of neurons is damaged.

This damage impairs the signal transmission in the affected nerves. Decreased arousal conduction can lead to sensory, motor and perceptual disorders.

The process of myelination requires migration, proliferation and differentiation of so-called oligodendrocyte progenitor cells (OPC). It is affected by extracellular matrix proteins, which consist of a network of glycoproteins and proteoglycans.

Dr. Juliane Bauch and Professor Andreas Faissner discovered that tenascin C reduces the amount of myelin membrane formed. It also has an inhibitory effect on OPC differentiation.

Structurally, Tenascin R has an inhibitory effect on the formation of myelin membranes in vitro. It also plays a supporting role for the CD68 protein, which causes inflammatory processes.

Anatomical drawing of the brain and cranial nerves
Multiple sclerosis (MS) is a disease in which the insulating shells of nerve cells in the brain and spinal cord are damaged. Pictured: Anatomical drawing of the male brain and cranial nerves.
Hulton-Archiv / Getty Images

“Our findings are an opportunity for new research strategies for demyelinating diseases such as MS,” Bauch said.

“The extracellular matrix has a huge effect on the formation of new myelin membranes. This could become an important research goal in the future. “

International research has not yet determined the cause of the destruction of myelin membranes.

“The human body has several mechanisms to compensate for some of the damage caused to cells.”

Researchers at Ruhr University treated mice with a drug that destroys the myelin membrane. They compared the regeneration process of these mice at the end of treatment with the progress of genetically engineered relatives who lacked key proteins.

The research found that mice lacking Tenascin C and Tenascin R were able to repair their myelin membrane more quickly.

Bauch and Faissner conduct research at the Cytomorphology and Molecular Neurobiology of Ruhr University.

When the university was founded in 1962, it was the first new public research institution in Germany after World War II.

MS was first described in 1868 by the French neurologist Jean-Martin Charcot.

According to the Global Burden of Disease 2015 study, MS affected an estimated 2.3 million people worldwide in 2015, and approximately 18,900 people died of MS this year. This is a significant increase since 1990, when about 12,000 people diagnosed with MS died of the disease.

The cause of MS is still unclear. The basic mechanism is thought to be either destruction by the immune system or failure of myelin-producing cells.

Possible causes include genetics and environmental factors such as viral infections.

Life expectancy is five to ten years lower than in the unaffected population.

This story was provided by Newsweek to Zenger News.

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