Myelin for brain rejuvenation
Every day new cells are formed in the brain in response to microtrauma, physical activity and mental activity. Glial cells, and in particular the precursors of oligodendrocytes, are very sensitive to external signals. They are able to find damage and form new myelin, which provides metabolism and rapid transmission of electrical impulses along the nerve. However, with age, less myelin is formed in response to external factors, and this is due to the intellectual and motor deficits observed in older people. Violation of myelin formation is also characteristic of neurodegenerative diseases, for example, multiple sclerosis or Alzheimer's disease, being one of the reasons for their progression.
The Neuroscience Initiative group at the Center for Advanced Research at the City University of New York has identified the ten-eleven-translocation 1 (TET1) enzyme as an important component for myelin repair. A study published in the journal Nature Communications showed that TET1 modifies DNA in the progenitor cells of oligodendrocytes so that they can form new myelin in response to the damaging effects of external factors.
In experiments on mice, the researchers found that the level of TET1 gradually decreased in older individuals, and because of this, DNA could no longer be modified in such a way as to provide the formation of functional myelin.
In young mice (left), TET1 is active in oligodendroglial cells, especially after injury, and this leads to the formation of new myelin and healthy brain function. In old mice (right), an age-related decrease in TET1 levels impairs the ability of oligodendroglial cells to form functional myelin.
The authors have shown that DNA modifications induced by the TET1 enzyme in young adult mice are necessary for healthy interaction between various cells of the central nervous system and to ensure their normal functioning. When young adult mice were genetically modified with TET1, making it non-functional, glial cells were not able to produce myelin; the animals showed changes characteristic of older individuals.
Thus, the age-related decline in TET1 function in the elderly may explain the inability of cells to form new myelin. The authors are convinced that studying the effects of aging on glial cells under normal conditions and in people with neurodegenerative diseases will help develop strategies for the treatment of disabling diseases such as multiple sclerosis and Alzheimer's disease.
This discovery is also important for the development of technologies to rejuvenate the aging brain in healthy people. Currently, studies are underway on old mice that are elevated TET1 levels to determine whether this molecule can trigger the formation of new myelin and promote proper communication between brain cells. The long–term goal of the research group is to promote the restoration of cognitive and motor functions in healthy elderly people and patients with neurodegenerative diseases.
Article by S.Moyon et al. TET1-mediated DNA hydroxymethylation regulates adult remyelination in mice published in the journal Nature Communications.
Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru Based on the materials of the Advanced Science Research Center at The Graduate Center of the City University of New York: Researchers Identify A Molecule Critical to Functional Brain Rejuvenation.