Mouse Study by Society-Funded Team Pinpoints Important Molecule in Myelin Repair
June 8, 2021
Researchers at the City University of New York’s Neuroscience Initiative Advanced Science Research Center and their international collaborators have pinpointed a molecule, called ten-eleven-translocation 1 (TET1), that is active in myelin-making cells especially after injury, and is crucial to the formation of new myelin. Myelin is the substance that surrounds nerve fibers and is a target of the immune response that occurs in multiple sclerosis. In older mice – or in younger, genetically modified mice – TET1 levels declined and myelin formation was impaired. Aging is emerging as one of the factors that may eventually limit natural myelin repair in people with MS.
This team is studying TET1 further to determine whether strategies targeting this molecule can help to restore function lost to age, or to MS and other diseases. This study is partly funded by the National MS Society through a postdoctoral research fellowship.
Read more from City University of New York
"TET1-mediated DNA hydroxymethylation regulates adult remyelination in mice," by (Society research fellow) Sarah Moyon, Rebecca Frawley, Damien Marechal, Dennis Huang, Katy L. H. Marshall-Phelps, Linde Kegel, Sunniva M. K. Bøstrand, Boguslawa Sadowski, Yong-Hui Jiang, David A. Lyons, Wiebke Möbius & Patrizia Casaccia, was published in
Nature Communications on June 7, 2021 (volume 12, Article number:3359) and can be read by anyone without a subscription.
Multiple sclerosis is an unpredictable disease of the central nervous system. Currently there is no cure. Symptoms vary from person to person and may include disabling fatigue, mobility challenges, cognitive changes, and vision issues. An estimated 1 million people live with MS in the United States. Early diagnosis and treatment are critical to minimize disability. Significant progress is being made to achieve a world free of MS.
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