Israeli Study Reveals Myelin's Role in Brain Energy Conservation

A new study from Ben-Gurion University of the Negev in Israel suggests that myelin, the fatty sheath surrounding nerve cell axons, plays a crucial role in conserving energy within the brain, not just in speeding up nerve signal transmission as previously understood. Researchers found that myelin reduced the energy required for nerve signal transmission by approximately half in thin axons within the brain's gray matter, with only a minimal increase in signal speed.

The study, led by doctoral student Oron Kotler and Professor Ilya Feydman from the Faculty of Health Sciences, examined thin axons in mouse brain gray matter. Using advanced imaging, electrical measurements, and computational models, they compared myelinated and unmyelinated axons. The results showed that while signal speed was nearly identical (around 0.32 meters per second) in both groups, the energy cost for signal transmission was significantly lower in myelinated axons.

This energy saving is attributed to a reduction in sodium ion entry into the axon during signal transmission. Myelin appears to limit this influx, thereby decreasing the metabolic cost for the cell to restore its chemical and electrical balance. The researchers propose that in the gray matter, myelin acts as an electrical filter, facilitating efficient signal transmission while preserving the neuron's energy and stability.

Professor Feydman explained that myelin in the gray matter organizes electrical currents at a nanoscale, enabling efficient signaling and maintaining the proper function of ion channels and pumps. This finding highlights a potential difference in myelin's function between the central and peripheral nervous systems.

The implications for diseases like multiple sclerosis, where myelin is damaged, are significant. The study suggests that myelin loss might not only impede signal transmission but also impose an increased energy burden on nerve cells, potentially contributing to functional impairment and degeneration. However, the researchers emphasize that this is basic research conducted on mice and computational models, and further studies are needed to confirm these mechanisms in humans and explore potential therapeutic applications.