The real cure for multiple sclerosis will come out of research like this.
The current issue of the journal Science(November 5) marks a turning point in research on the brain. This event is fascinating not only for the wealth of new information about how the brain functions and how it fails in mental and neurological illness, but equally as a rare display of a field of science changing course. Such transitions are the lore of scientific history, but rarely do we have the opportunity to witness such pivotal moments in real time.
.....................
.......................
The third important function of glia is to form the electrical insulation on nerve fibers (axons), which is essential for high speed transmission of electrical impulses. The importance of this insulation, called myelin, is clearly seen in people who suffer from multiple sclerosis, an autoimmune disorder that attacks the myelin sheath on axons, which leaves these people with serious impairments in sensory and motor function. Inside the brain and spinal cord, glial cells resembling cellular octopuses wrap up to 150 layers of compacted membrane around axons, much like electrical tape. The core of the brain—half its bulk—is comprised of millions of tightly bundled axons insulated with myelin. This brain region is called "white matter," because the color of myelin tints this brain tissue white. Although of little interest in the past, white matter is the newest area of research on learning. In the rest of the body, glial calls called Schwann cells, which resemble flattened pearls strung up on axons, form this vital insulation.
My article in this issue explains the sea change in thinking about white matter in the brain. Traditionally myelin was primarily of interest to those concerned with demyelinating disease, but new brain imaging research and cellular research showing that myelinating glia sense electrical activity in axons, is revealing that white matter changes during learning. The formation of myelin can be controlled by electrical impulse activity, and thus by experience. When a bare axon becomes myelinated, the speed of impulse transmission through the fiber increases roughly 50 times. The increased transmission speed will have profound effects on information processing in that neural circuit. A remarkable thing about the human brain is that it continues to form myelin through childhood, adolescence, and at slower rates into early adult life. After age 50, myelin begins to be lost in parallel with the normal gradual decline in cognitive function with aging. This new research is expanding thinking about the mechanisms of learning beyond the synapse, to include the transmission of information through the entire network involved in carrying out a complex cognitive function. White matter changes are seen by brain imaging after learning new skills, ranging from playing computer games, to golf, to reading, to juggling, to playing the piano, and the molecular signals from axons that control development and formation of myelin in response to electrical impulse activity are being identified.
The article by Ben Emery, of the Florey Neuroscience Institutes in Melbourne, Australia, summarizes what is known about the mechanisms controlling development of oligodendrocytes and myelin. Both chemical signals from the environment, and internal controls regulate development of oligodendrocytes from immature "progenitor cells". These oligodendrocyte progenitor cells (OPCs), are of intense interest, because new research shows that they can transform not only into mature oligodendrocytes, but also into astrocytes and neurons under the proper conditions. These are the cells that are now being transplanted into patients with spinal cord injury in experimental studies to cure paralysis. Most intriguingly, neurons form synapses onto these cells for reasons that are not understood. A possibility that is hotly pursued is that synaptic communication could instruct these cells to form myelin, although there is no evidence for this as yet. (Also, research just published from my lab in the October 5 issue of Science Signaling reveals a new mechanism for axons to release neurotransmitter without synapses. This is especially important in communicating with myelinating glia, which are far removed from synapses.) Emery sees the major challenge of the future will be in translating our new knowledge into new therapies to treat diseases like multiple sclerosis.