There are many neurodegenerative diseases, one of the worst being multiple sclerosis (MS).In MS and similar diseases, the myelin, the sheath that protects the connections between brain cells, is damaged, and as a result, the connections themselves are destroyed.The cause and mechanism of this phenomenon are unknown, although it is most often believed to be an autoimmune disease.In patients with multiple sclerosis, myelin repair fails for reasons we don't know yet, says Robyn Klein, a professor of medicine and neurobiology at the Washington University School of Medicine in St.Louis.It's important to understand the nature of the problem, because unbuilt myelin sheaths put you at drastically greater risk of serious harm to your nervous system.While not getting very close to understanding the causes of myelin loss, hope has emerged for an effective way to rebuild the myelin sheaths that would stop or even reverse the progression of the disease.Such hope was provided by a protein called CXCR4, so far known to participate in the processes of shaping the brain in children.It was shaping, not repairing, which is why the discovery amazed scientists at the University of Washington.The fact that damage to the brain causes an increase in the number of cells that produce the CXCR4 protein led to the trail.So it was considered worth looking at.The studies were carried out in the mouse model of the SR.Such models usually mimic the effects of the disease by triggering inflammatory processes, but this approach, according to the authors of the research, makes it difficult to focus on how the regeneration of the myelin sheaths takes place.Instead, Dr. Klein and the lead author, Dr. Jigisha Patel, used a non-inflammatory model by feeding in the food the factor that causes the death of oligodendrocytes, the cells that form myelin.After six months of a diet enriched with oxalic acid bis (cyclohexylidene hydrazide) and cell death, the corpus callosum - the nerve connection between the brain's hemispheres - was stripped of its protective sheath.When the factor was then removed from the diet, new cells began to migrate to the myelin repair site, becoming new oligodendrocytes.When can stem cells no longer repair the damage?However, the study began earlier, when dying oligodendrocytes triggered processes of interest to researchers and activated other cells, prompting them to produce inflammatory factors.The number of CXCR4 receptors peaked within six weeks.If the mice were fed oxalic acid bis (cyclohexylidenehydrazide) (C14H22N4O2) for more than 12 weeks, the levels of the inflammatory factor and its receptors dropped significantly.After 12 weeks, the mice were no longer able to rebuild the myelin sheath.This suggests a link between myelin restoration and the CXCR4 protein.It was also shown that cells destined to become mature oligodendrocytes had high concentrations of the protein of interest.Blocking its activation or limiting its production in cells also made it impossible to rebuild myelin.Clearly, the precursor cells must stop multiplying before they can migrate to the target, and CXCR4 plays a role in that, Dr. Klein explains.It also appears to be important for the ability of cells to transform into mature oligodendrocytes and form myelin.There are plans to study genetically modified mice and use advanced imaging techniques to accurately determine the relationship between myelin damage and loss of intercellular connections.We don't know yet whether this myelin repair procedure is broken or ineffective in MS patients, says Dr. Klein.But the very intriguing idea is to turn on something in the brain that it can use to heal itself with its own resources.Source: Washington University School of Medicinemultiple sclerosis sclerosis multiplex myelin neurons oligodendrocytes CXCR4 Robyn Klein Jigisha Patel Washington UniversityA request to those who know medicine: what is the Polish word for "cuprizone" ("factor causing the death of oligodendrocytes")?I have not found a Polish translation.(Science: chemical) copper chelator that inhibits monoamine oxidase and causes liver and brain damage.Pharmacological action: chelating agents, monoamine oxidase inhibitors.chemical name: Ethanedioic acid, bis (cyclohexylidenehydrazide)http://www.biology-online.org/dictionary/CuprizoneJust Coupon or Coupon.RSS Privacy Policy |Training