German scientists are cautiously optimistic about new treatment options for multiple sclerosis after decoding the functions of two crucial proteins.
Multiple sclerosis (MS) is a disease in which the insulating linings of nerve cells in the brain and spinal cord are damaged. There is no known cure and treatments attempt to improve function after an attack and prevent further attacks.
Nearly 3 million people worldwide suffer from MS.
Researchers from the Ruhr University in 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 disease in which the myelin sheath of neurons is damaged.
This damage impairs signal transmission in the affected nerves. Reduced conduction of excitation can lead to sensory, movement and perception disturbances.
The process of myelination requires the migration, proliferation and differentiation of progenitor cells called oligodendrocytes (OPCs). It is influenced by the proteins of the extracellular matrix, made up of a network of glycoproteins and proteoglycans.
Doctor 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.
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 CD68 protein, which causes inflammatory processes.
“Our results are a window of opportunity for new research strategies for demyelinating diseases such as multiple sclerosis,” Bauch said.
“The extracellular matrix has a huge influence on the formation of new myelin membranes. This could become an important research goal in the future.
The cause of the destruction of the myelin membrane has not yet been determined by international research.
“The human body has several mechanisms to compensate for some of the damage caused to cells.”
Scientists from 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 modified congeners lacking essential 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 Ruhr University Cytomorphology and Molecular Neurobiology.
When it was established in 1962, the university was the first new public research institution in Germany after World War II.
MS was first described in 1868 by French neurologist Jean-Martin Charcot.
According to the Global Burden of Disease 2015 study, MS affected around 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 myelin-producing cells.
Possible causes include genetics and environmental factors such as viral infections.
Life expectancy is five to ten years less than that of the unaffected population.
This story was provided to Newsweek by Zenger News.
#Protein #study #pave #multiple #sclerosis #therapy