The brain consumes substantial energy, and research from Ben-Gurion University of the Negev has identified how myelin contributes to that efficiency. Scientists at the institution found that myelin, the protective layer surrounding nerve fibers, primarily functions as an energy-conservation mechanism rather than as a signal accelerator, reducing the energy cost of brain signaling by 50 percent.

The discovery may advance understanding of Multiple Sclerosis and other myelin-related diseases by clarifying how myelin loss influences both nerve signaling and metabolic balance in the brain. Such insights could inform future treatments focused on protecting neurons, maintaining myelin function, and alleviating metabolic stress from myelin damage.

Published in the Proceedings of the National Academy of Sciences, the research challenges conventional understanding of myelin's role in the brain. Rather than primarily accelerating nerve signals, myelin in the brain's cortical gray matter primarily reduces the energy required for neuronal communication while sustaining normal brain function.

PhD student Oron Kotler conducted the study under Prof. Ilya Fleidervish from the Department of Physiology and Cell Biology, alongside collaborators from Soroka University Medical Center, the Weizmann Institute of Science, and New York Medical College.

Myelin is the fatty insulating layer around axons that help electrical signal transmission. In peripheral nerves, myelin substantially increases signal speed while lowering energy use. Its function within the brain's gray matter, where densely packed neurons create intricate networks, had remained unclear.

Using imaging, electrical recording, and computer modeling, researchers compared cortical nerve fibers with and without myelin. Myelination produced no significant change in signal speed; both types transmitted signals at approximately 0.32 meters per second.

Energy consumption showed the critical difference. Myelinated axons allowed 50 percent less sodium entry during electrical signaling. Since neurons expend cellular energy as adenosine triphosphate to remove sodium and restore chemical balance, this reduction cuts signaling energy costs in half.

Cortical myelin differs structurally from peripheral myelin. Rather than forming long, sealed segments that maximize speed, cortical myelin consists of shorter insulated sections with more flexible junctions, permitting energy conservation while preserving electrical function.

Understanding cortical myelin's energy-saving purpose could reshape MS research. Myelin damage may increase neuronal energy demands alongside disrupting signals, suggesting therapies targeting both myelin protection and neuronal metabolism. The findings may guide drug development by establishing energy regulation as a treatment focus, with future approaches aiming to preserve myelin, protect axons, and help neurons maintain chemical balance after injury.

The research may additionally offer insights for developing energy-efficient artificial intelligence and brain-inspired computing by demonstrating how the brain balances performance with minimal energy use.