Myelin is a substance rich in lipids (fatty substances) and proteins that forms layers around the nerve fibers and acts as insulation. The nerve can be likened to an electrical cable; the axon, or nerve fiber that transmits the nerve impulse, is like the copper wire; and the myelin sheath is like the insulation around the wire. Myelin is present in both the central nervous system (CNS) and the peripheral nervous system (PNS), but MS affects only the CNS myelin.
The CNS (the brain, spinal cord and optic nerves) is made up of several different components:
- Gray matter contains the cell bodies of the nerves.
- White matter contains nerve fibers coated with myelin.
- Supporting cells form a supporting network.
PNS nerve cells perform two major functions:
- Sensory neurons collect information about the body’s internal and external environment and convey it to the CNS.
- Motor neurons carry instructions from the CNS to the glands and muscles.
CNS and PNS Myelin Are Produced by Different Cells
CNS myelin is produced by special cells called oligodendrocytes. PNS myelin is produced by Schwann cells. The two types of myelin are chemically different, but they both perform the same function—to promote efficient transmission of a nerve impulse along the axon.
The myelin layer is segmented and there are small nodes between the segments that are naturally unmyelinated. As chemical ions pass in and out of the axons, the electrical current they generate is conducted down the nerve, jumping from node to node. Myelin prevents the current from leaking out of the nerve at inappropriate points and decreases the electrical resistance of the nerve. This helps make sure the nerve impulse is conducted efficiently.
Abnormal Immune Reaction Believed to Attack Myelin
An abnormal immune reaction in MS is believed to initiate an attack on the myelin, resulting in lesions—bare spots and scarred areas along the nerve. Conduction of the nerve impulse is then slowed or halted, producing the neurologic signs and symptoms of MS. Destruction of myelin, a process known as demyelination, can also lead to “cross-talk” between nerves—abnormal nerve-to-nerve signaling, which also may produce symptoms.
Some Myelin Repair Occurs Naturally
Scientists have discovered that the body heals some lesions naturally by stimulating oligodendrocytes in the area—or recruiting young oligodendrocytes from further away—to begin making new myelin at the damaged site. Research is underway to identify the molecular signals that the body uses to activate the oligodendrocytes so that those signals can be mimicked to stimulate additional repair. Scientists are also studying certain proteins known as growth factors to identify their potential role in myelin repair.
As scientists work to stimulate myelin repair, they are also focusing their attention on several properties of myelin that work to inhibit this repair. Eventually, they may develop therapies to stop these components of myelin from inhibiting the repair process.
Specific Approaches to Myelin Repair
Scientists are investigating several different strategies for stimulating the repair of myelin.
- Antibodies (immune proteins that attach to specific molecules) have been successfully used to stimulate myelin repair in rodents with an MS-like disease. Based on the outcomes of this research, preliminary testing for safety in people with MS is planned.
- Efforts are also being made to surgically replace damaged oligodendrocytes and nerve cells.
Scientists are working to identify potential sources of replacement cells for those that are damaged by MS. Possible sources include: skin-derived cells, bone marrow and umbilical cord blood cells, fetal cells, adult brain cells, and Schwann cells from the PNS. The usefulness of these replacement cells will depend on finding or creating the signals needed to stimulate their transformation and growth into healthy new cells.
The Future of Myelin Repair
The Society has provided $15.6 million to four teams in the U.S. and Europe to lay the groundwork for clinical trials in nervous system repair by 2010. This funding level allows scientists to form new alliances, to re-tool and hone their scientific and clinical skills for this very specific effort, to attract more “heads and hands” to the problem, and to utilize the best possible technologies to promote tissue repair.