Scientists in Germany are cautiously optimistic regarding new therapeutic options for multiple sclerosis following decoding the functions of two crucial proteins.
Multiple sclerosis (MS) is a disease in which the insulating coverings of nerve cells in the brain and spinal cord are damaged. There is no known cure, and treatments attempt to improve function following an attack and prevent new attacks.
Almost 3 million people worldwide suffer from MS.
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Now researchers at the Ruhr University Bochum have announced a breakthrough in the study of the proteins tenascin C and tenascin R.
MS is the most common demyelinating or nervous system disorder in which the myelin sheath of neurons is damaged.
This damage impairs signal transmission in the affected nerves. The reduction in the conduction of excitation can lead to sensory, movement and perception disorders.
The myelination process requires the migration, proliferation, and differentiation of so-called oligodendrocyte progenitor cells (OPCs). It is influenced by proteins of the extracellular matrix, which consists 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 the differentiation of OPCs.
The structurally similar Tenascin R exerts an inhibitory effect on the formation of myelin membranes in vitro. It also has a supporting role for the protein CD68, which causes inflammatory processes.
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“Our findings are a window of opportunity for new research strategies for demyelinating diseases such as MS,” said Bauch.
“The extracellular matrix has an enormous influence on the formation of new myelin membranes. It might become an important research goal in the future.”
The cause of myelin membrane destruction has not yet been determined by international research.
“The human organism has several mechanisms to compensate for some of the damage caused to the cells.”
The scientists from the 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 conspecifics that lacked the crucial proteins.
The research found that mice lacking Tenascin C and Tenascin R were able to repair their myelin membrane faster.
Bauch and Faissner conduct research at the Ruhr University’s Cytomorphology and Molecular Neurobiology.
When it was founded in 1962, the university was the first new public research institution in Germany following the Second World War.
MS was first described in 1868 by 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 around 18,900 people died from MS that year. This is a significant increase from 1990, when around 12,000 people diagnosed with MS died from the disease.
The cause of MS is still unclear. The underlying mechanism is thought to be either destruction by the immune system or failure of the myelin-producing cells.
Possible causes include genetics and environmental factors such as viral infections.
Life expectancy is five to ten years lower than that of the unaffected population.
This story was provided to Newsweek by Zenger News.
