The recent advancements in technology and research related to cellular medicine revealed a correlation between myelin sheath, a fatty coating responsible for insulating nerve fibers from electrical signals. In this regard, a team of scientists from the University at Buffalo pinpointed a different mechanism that was responsible for preventing repairing of myelin sheath in case of multiple sclerosis. The proposed mechanism has been identified to be effective in further stopping the production, growth as well as the development of progenitor cells into oligodendrocytes, the key cells in the formation of the myelin sheath. Further to which, the in-depth analysis in the same direction, confirmed that due to further stoppage of the progression of the cell cycle, the progenitor cells are deactivated. This phenomenon of deactivation is called as pathological quiescence.

It should further be noted that hierarchy wise, the progenitor cells are the descendants of stem cells that are committed towards particular cellular lineage but are not distinctively matured to form the tissue-specific cells. However, progenitors cells can also not be dividing indefinitely just like their ancestors.  Although various investigations have been presented in this regard, one prominent amongst them is the study published in the journal of cells and have pinpointed towards Paired related Homeobox protein 1 i.e. PRPX1 for switching on the mechanism of deactivation.

What exactly Multiple Sclerosis is?

Multiple sclerosis is a progressive neurodegenerative disorder, characterized by loss of myelin sheath that acts as insulating material further protecting neurons from external shocks of electrical signals. This destruction of the myelin sheath is further responsible for halting a smooth passage of sensory information from the central nervous system to muscles; especially due to massive destruction of nerve fibers. Studies have been able to know that some of the symptoms like extreme fatigue, difficulties in walking, reduction in the visual acuity and altered sensation are generally prevalent, and have to be checked for. It has also been evaluated that the exhibition of these symptoms are fairly progressive in nature and are estimated to be troubling around 2.3 million people worldwide.

What can prevent myelin repair?

As discussed previously, PRPX1 is confirmed to be responsible for deactivating the growth as well as the development of progenitor cells, through bringing in important epigenetic changes. The defect was practically being demonstrated in the mouse model of childhood leuko dystrophy further destroying the old myelin sheath and preventing the formation of a new one. The study could reveal new pathways that can be targeted to stimulate the production of mature myelin-producing cells.

Thus, scientists are pursuing the idea that perhaps can identify a definitive treatment leading to complete cure for multiple sclerosis, which can be achieved through overcoming pathological quiescence of myelin sheath.


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