Author: Benderev Chris
Date: July 2007
Researchers at the Weizmann Institute of Science in Israel recently released findings in Nature Neuroscience that reveal new crucial aspects of nerve cell communication. Their discovery of proteins that signal the start of myelination,a process that allows faster communication within the nervous system,may allow future researchers to develop cures for neurologically degenerative disorders such as multiple sclerosis (MS).
Professor Elior Peles, his graduate student Ivo Spiegel, and other collaborating researchers examined communication between glial cells and axons with special attention paid to myelination,the process by which myelin is formed.
When a nerve cell, also known as a neuron, sends a message, it dispatches an electrical impulse,the currency of the commerce of the nervous system,that travels down a long and narrow branch called an axon. To expedite the impulse, often large portions of axons are covered with thick insulating sheaths known as myelin. The electrical impulse can traverse the myelinated portions of axons almost instantly, greatly reducing the time it takes for signals to get to, from, and around the brain. Glia are the cells responsible for laying down the myelin on the axons. When the glia, axons or myelin are not functioning properly, cell communication is affected, often slowing or degenerating all together.
Professor Peles and his colleagues studied the interaction of glia and axons during myelination and found two related proteins, Necl1 and Necl4, present on the surfaces of axons and glia, respectively. The scientists found that when the proteins are isolated from glia and axons and are placed in tight proximity to each other in a container, Necl1 and Necl4 bind closely together.
What's more, when axons and glia draw near to each other and the two proteins bind, chemical messages are sent to the inside of the glia and axons involved, ordering them to begin changes that are essential to the formation of myelin. In situations where researchers inhibited the connection of Necl1 and Necl4, or used glia lacking Necl4 entirely, myelination was slow to start and lagged significantly behind the control group.
Considering the fact that current drugs for MS and other neurodegenerative disorders can only slow, not stop or reverse, the degradation of myelin, Professor Peles found these new findings hopeful. He said, "if we can understand the mechanisms that control the process of wrapping the axons by their protective sheath, we might be able to recreate that process in patients."