Jerusalem, 20 October, 2025 (TPS-IL) — israeli scientists have identified a biological mechanism that significantly boosts the production of myelin, the fatty substance that insulates nerve fibers and enables rapid transmission of electrical signals between neurons. The discovery could pave the way for new treatments for severe neurological disorders, including multiple sclerosis, Alzheimer’s disease, and certain neurodevelopmental syndromes.
The study, conducted in the laboratory of Prof. Boaz Barak of the Sagol School of Neuroscience and the School of Psychological Sciences at Tel Aviv University, was led by Dr. Gilad Levy. The team collaborated with Dr. Asaf Marco from the Hebrew University of Jerusalem, Prof. Inna Slutsky and Prof. Yaniv Assaf from Tel Aviv University, Prof. Elior Peles from the Weizmann Institute of Science, and Prof. Hauke Werner from Germany. The findings were published in the peer-reviewed journal, Nature Communications.
When myelin is damaged, nerve signals slow down, leading to conditions like multiple sclerosis, Alzheimer’s disease, and some developmental disorders. Increasing or repairing myelin could help restore nerve function.
“In this study, we focused on the cells that produce myelin in both the central and peripheral nervous systems,” Barak explained. “Specifically, we investigated the role of a protein called Tfii-i, known for its ability to increase or decrease the expression of many genes crucial for cell function. While Tfii-i has long been linked to abnormal brain development, its role in myelin production had not been studied until now.”
The researchers found that Tfii-i acts as a ‘biological brake’ that inhibits myelin production in the relevant cells. Based on this insight, they hypothesized that reducing Tfii-i activity in myelin-producing cells might increase myelin output.
To test the idea, the team used advanced genetic engineering in mice, selectively eliminating Tfii-i expression only in myelin-producing cells while leaving all other cells unchanged. These genetically modified mice were then compared to normal mice across multiple measures, including levels of myelin proteins, the structure and thickness of the myelin sheath surrounding axons, the speed of nerve signal conduction, and motor and behavioral performance.
Levy said, “We found that in the absence of Tfii-i, the myelin-producing cells generated higher amounts of myelin proteins. This resulted in abnormally thick myelin sheaths, which enhanced the conduction speed of electrical signals along the neural axons. These improvements translated into a significant enhancement of the mice’s motor abilities, including better coordination and mobility, along with other behavioral benefits.”
The discovery of Tfii-i’s role in myelin production could lead to therapies for a range of neurological and developmental disorders. In multiple sclerosis, where the immune system attacks myelin, reducing Tfii-i activity could help repair damaged nerve fibers and improve motor function. In Alzheimer’s disease, boosting myelin production may slow cognitive decline and support brain connectivity. Similarly, in neurodevelopmental disorders such as Williams syndrome and autism spectrum disorders, regulating Tfii-i could help normalize neural development and enhance cognitive and motor outcomes.
Barak said, “We believe this fundamentally new approach holds great therapeutic potential.”
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