Researchers identify a key molecule for functional brain rejuvenation


In young adult 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), age-related decline in TET1 levels affects the ability of oligodendroglial cells to form new functional myelin. The authors are currently investigating whether increasing TET1 levels in older mice could rejuvenate oligodendroglial cells and restore their regenerative functions. Credit: Sarah Moyon

Recent studies suggest that new brain cells are formed every day in response to injury, exercise, and mental stimulation. Glial cells, and in particular so-called oligodendrocyte progenitors, are very sensitive to external signals and lesions. They can detect changes in the nervous system and form new myelin, which surrounds the nerves and provides metabolic support and accurate transmission of electrical signals. However, as we age, less myelin is formed in response to external signals, and this progressive decrease has been related to age-related cognitive and motor deficits detected in older people in the general population. Impaired myelin formation has also been reported in elderly people with neurodegenerative diseases such as multiple sclerosis or Alzheimer’s and identified as one of the causes of their progressive clinical deterioration.

A new study by the Neuroscience Initiative team at the Advanced Science Research Center at the Graduate Center, CUNY (CUNY ASRC) has identified a molecule called ten-eleven-translocation 1 (TET1) as a necessary component of repair. The research, published today in Communications on Nature, shows that TET1 modifies DNA specifically in adult brains so that they can form new myelin in response to an injury.

“We designed experiments to identify molecules that could affect brain rejuvenation,” said Sarah Moyon, Ph.D., research assistant professor at the CUNY ASRC Neuroscience Initiative and lead author of the study. “We have found that TET1 levels progressively decrease in older mice, and as a result, DNA can no longer be properly modified to ensure the formation of functional myelin.”

Combining complete genome sequencing bioinformatics, the authors demonstrated that TET1-induced DNA modifications in young adult mice were essential to promote healthy dialogue between at the plant and to ensure proper operation. The authors also demonstrated that young adult mice with a genetic modification of TET1 in myelin-forming glial cells were not able to produce functional myelin and therefore behaved like older mice.

“This new age-related decline in TET1 may explain the inability of older people to form new myelin,” said Patrizia Casaccia, founding director of the CUNY ASRC Neuroscience Initiative, a professor of Biology and Biochemistry at The Graduate Center. CUNY, and the study’s lead researcher. “I believe that studying the effect of aging on glial cells under normal conditions and in people with neurodegenerative diseases will ultimately help us design better therapeutic strategies to slow the progression of devastating diseases such as multiple sclerosis and l ‘Alzheimer’s’.

The findings could also have important implications for the molecular rejuvenation of aged brains in healthy individuals. Future studies are underway aimed at increasing TET1 levels in older mice to define whether the molecule could rescue the formation of new myelin and promote proper neuro-glial communication. The long-term goal of the research team is to promote the recovery of cognitive and motor functions in the elderly and in patients with .

Scientists discover the role of a protein in the production and survival of myelin-forming cells

More information:
Communications on Nature (2021). DOI: 10.1038 / s41467-021-23735-3

Citation: Researchers identify a key molecule for functional brain rejuvenation (2021, June 7) recovered on June 7, 2021 at rejuvenation.html

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